This study was to investigate the effect and the underlying mechanism of DG on the hepatotoxicity induced by Con A.In this study,a concanavalin A (Con A)-induced hepatitis mouse model was used to examine the effect of DG on hepatic injury.DG(58.5 mg/kg),silymarin (36.4 mg/kg) and bicyclol (9.75 mg/kg) equivalent to clinical dosage were orally administered to mice once daily for 7 consecutive days before Con A challenge.After that,blood samples were collected for serological detection,and histological analysis was carried out by hematoxylin-eosin staining.In order to investigate the molecular mechanism of DG’s protective effect,the serum-drug incubation assay,immunohistochemistry and western blot were conducted.Hematoxylin-eosin staining showed that DG pre-treatment prevented Con A-induced liver structural damage in ICR mice.We also observed the reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities.However,the serum-drug incubation assay indicated that DG cannot directly attenuate ALT and AST levels.Meanwhile,experimental results proved that DG pretreatment down-regulates cleaved Caspase-3,cleaved PARP,ratio of BAX/BCL-2 expression level and expression of TGF-β1,COX-2,IL-6,TNF-α,IFN-γ inflammatory mediators.Taken together,DG can inhibit Con A-induced hepatic injury by inhibition of apoptosis and inflammation.

This study aimed to understand the protective effects of total alkaloids from lotus leaves (TAL) on acute liver injury induced by acetaminophen (APAP) in mice and the potential mechanisms.Mice were randomly divided into 4 groups,i.e.,the normal group,the model group,the TAL low-dosage group (30 mg/kg) and the TAL high-dosage group (100 mg/kg).Animals received TAL through gavage for 7 consecutive days.Then,except the normal group,other groups received APAP (300 mg/kg) by intraperitoneal injection to provoke acute liver injury.Serum and livers of mice were collected 12 h later and subjected to further experiments.Our results showed that as compared to the model group,TAL significantly decreased activities of ALT and AST in the serum and contents of TNF-α,IL-1β,IL-6 and MDA in the liver.In addition,TAL dose-dependently elevated hepatic levels of SOD,CAT,GSH-Px and GSH.Moreover,APAP-induced liver histopathological changes were dramatically alleviated by TAL.Mechanistically,TAL considerably boosted AMPK phosphorylation,induced nuclear translocation of Nrf2 and promoted expression of HO-1 and GCLC.In conclusion,this study revealed that TAL has the capacity of ameliorating APAP-induced acute liver injury,and the underlying mechanisms are related with the activation of hepatic AMPK/Nrf2 cascade.

To investigate the protective effect of Broussonetiae Fructus on acetaminophen-induced liver injury in rats and the regulatory effects on peroxisome proliferators activated receptor α (PPAR-α),peroxisome proliferators activated receptor γ (PPAR-γ),and C-Ros oncogene 1 (ROS1).50 SD rats were randomly divided into normal group,model group,silymarin group (44 mg/kg),Broussonetiae Fructus high and low dose groups (4.2，1.05 g crude drug/kg) with 10 rats in each group.The rat model of drug-induced liver injury was induced by acetaminophen (1.2 g/kg) orally once daily for 30 days.At the same time of modeling,normal group and model group were given saline infusions by gastric lavage,while the rest groups were given corresponding liquid infusions for 30 days.At the end of the experiment,the activities of AST,ALT,SOD,CAT and GSH-Px,and the contents of TBIL,DBIL,MDA and GSH in serum were measured.Part of the liver tissue was fixed with 4% paraformaldehyde solution,the pathological morphology of the liver was observed with HE staining,and the gene expression of PPAR-α and PPAR-γ were observed by RT-PCR,and the protein expression of ROS1 (C-Ros oncogene 1) was observed by immunohistochemistry.Our results showed that compared with the normal group,the levels of ALT,AST,TBIL and DBIL in rats of the model group were significantly increased,the content of MDA in serum and the gene expression of PPAR-γ in liver were increased,while the levels of SOD,GSH,GSH-Px and PPAR-α were decreased.Compared with the model group,different doses of Broussonetia Fructus could reduce the levels of ALT,AST,TBIL and DBIL,increase the levels of SOD,GSH,GSH-Px in serum,inhibit the gene expression of PPAR-γ and the protein expression of ROS1,and up-regulate the gene expression of PPAR-α.In conclusion,the results of this study suggest that Broussonetiae Fructus may have protective effect on the hepatic injury induced by acetaminophen in rats,and its mechanism may be related to the inhibition of oxidative stress and regulation the gene expression of PPAR-γ,PPAR-α,and the expression of ROS1 protein.

To explore the protective effect of Lycium barbarum polysaccharides (LBPs) on ethanol-induced hepatocyte injury.Crude polysaccharides (LBPs0) and different molecular weight ranges LBPs (LBPs1-LBPs4) were extracted and separated from Lycium barbarumsamples,human normal hepatocytes (L-02 cells) were used to evaluate the protective activity of LBPs on ethanol-induced hepatocyte injury:Cell activity was detected by MTT assay,the release of ALT,AST and LDH in cell culture was detected by colorimetry,and intracellular reactive oxygen species (ROS) were detected by DCFH -DA assay.The results showed that LBPs had no inhibition or promotion effect on cell proliferation between 0-200 μg/mL,and could protect ethanol-induced hepatocyte injury by increasing cell activity,reducing the release of ALT,AST and LDH,and inhibiting intracellular ROS production.The activity of LBPs in different molecular weight ranges was different,LBPs3 was the strongest,followed by LBPs4 and LBPs2,and LBPs1 was the weakest.In conclusion,LBPs can protect ethanol-induced hepatocyte injury,and LBPs3 with a molecular weight range of 5-10 kDa has the highest activity,the results of this experiment can provide experimental basis and theoretical guidance for the application and development of LBPs to protect liver injury functional food and drug.

To investigate the therapeutic effect and mechanism of Qi-Tonifying Decoction (Astragalus membranaceus and Atractylodes macrocephala) on hepatic fibrosis induced by CCL4 in rats.Hepatic fibrosis model was established by intraperitoneal injection of 40% carbon tetrachloride (CCL4) corn oil solution combined with high fat and low protein diet.The drugs were given to each group for 12 weeks.HE and Masson staining were used to observe the morphological changes of hepatic tissues.Biochemical analysis was used to detect liver function in serum.Enzyme-linked immunosorbent assay(ELISA) was used to detect collagen content in serum.The expression of TGF-beta 1,T beta R I,Smad3,Samd7,alpha -SMA and HGF in liver tissue was detected by RT-qPCR.After administration,Qi-Tonifying decoction and colchicine could reduce collagen deposition and improve liver function in rats,and its mechanism is related to inhibiting TGF-beta 1/Smad signaling pathway.

Auriculatone sulphate(AS)was a prodrug of auriculatone that is a natural hepatoprotective compound.In order to evaluate the hepatoprotective effect of AS,an acetaminophen(APAP)-induced acute liver injury model of mice was established by intraperitoneal administration of 300 mg/kg APAP.The hepatoprotective effect of AS(25 mg/kg)was initially evaluated by determining its inhibitory effect on the increases of serum alanine aminotransferase(ALT),aspartate aminotransferase(AST)and lactate dehydrogenase(LDH)induced by APAP.The protective effect of AS against oxidative damage was assessed by measuring the levels of malondialdehyde(MDA)and glutathione(GSH)and testing the activity of superoxide dismutase(SOD)in the liver tissue.Histochemical analysis of liver tissue was also conducted to evaluate the hepatoprotective effect of AS.The results showed that intravenous pretreatment with AS significantly prevented the liver tissue from APAP-induced injury,and retained the serum ALT,AST and LDH levels close to those of the control group(P<0.001).When compared with the APAP group,AS pretreatment significantly decreased the hepatic level of MDA(P<0.001),and increased the hepatic level of GSH as well as the activity of SOD(P<0.001).Histochemical examinations showed that AS treatment significantly improved the pathological changes of liver tissues.In conclusion,intravenous administration of AS effectively protected mouse against APAP-induced liver injury and the protection might involve its inhibition of liver tissue oxidative damage.

The study was to explore the antioxidant capacity of thyme essential oil and its potential protection effects on the liver of mice.The anti-oxidation activities of thyme essential oil were analyzed by DPPH· and ABTS·⁺ scavenging experiments.Besides,the acute liver injury model of Kunming mice by Thioacetamide (TAA) was also established,and the liver protection effects of thyme essential oil were assessed by determining the activity of ALT,AST and ALP in mice blood samples.After the homogenization of the liver tissue,the MDA,GSH contents and SOD,GSH-Px and CAT activities were further analyzed.The results suggested that thyme essential oil had significant anti-oxidation capacities and protection effects on the liver of the mice,especially when used at high doses.The study aimed to provide the theoretical foundation for the research and development of thyme essential oil.

In this experiment,a crude extract named as AWE was extracted by water extraction from Acalypha wilkesiana leaves,and then a polyphenol-enriched fraction was prepared by macroporous resin,designated as AWF.Based on the results of free radical scavenging activities of AWE and AWF in vitro,the hepatoprotective effects of AWF and the underlying mechanisms were further investigated by APAP-induced acute liver injury mice model.Results showed that the polyphenol contents in AWE and AWF reached 224.9±1.5 and 608.7±16.4 μg GAE/mg extract,respectively.AWF exhibited strong scavenging abilities on DPPH and ABTS free radicals,the IC₅₀s were 4.46 and 41.25 μg/mL,respectively.AWF (200 and 400 mg/kg·bw) pretreatment significantly alleviated APAP-induced acute liver injury,as evidenced by the decreased serum levels of ALT,AST,LDH,and MDA (P<0.05 or P<0.001),and the elevated activities of SOD,CAT,and GSH-Px (P<0.01or P<0.001),the results of which were further confirmed by the histopathological analysis.Moreover,AWF remarkably inhibited the activation of MAPKs and proapoptotic protein caspase-3/9,down-regulated the expression level of proapoptotic protein Bax and restored the expression level of antiapoptotic protein Bcl2.These results indicate that AWF possesses hepatoprotective effects against APAP-induced liver injury,which may be attributed to the antioxidant and antiapoptotic effects through the modification of MAPKs/apoptosis cascade reaction.

To study the hepatoprotective effects of the total flavonoids extracted from the dried root of Cyclea hypoglauca(Schauer)Diels(TFC)on mice with acute liver injury induced by carbon tetrachloride(CCl₄),and explore the mechanism based on oxidative stress,inflammatory response and toll-like receptor-4(TLR-4)/nuclear factor-kappa B(NF-κB)pathway.60 mice were randomly divided into normal group,model group,silymarin group(150 mg/kg),and TFC-low,medium,high dose groups(100,200,400 mg/kg).All mice were administrated by gavage once a day for 10 d with distilled water or corresponding dose of drugs(10 mL/kg).After 2 h of the last administration,the mice were injected intraperitoneally with 0.1% CCl₄ peanut oil solution(10 mL/kg)to induce the acute liver injury except the normal group.16 h later,the eye balls of mice were removed to take blood,and all mice were sacrificed to collect the liver tissue.Liver index was calculated based on body weight and liver weight of mice.Biochemical methods were used to measure the serum contents of alanine aminotransferase(ALT),aspartate aminotransferase(AST),alkaline phosphatasetotal(ALP),total bilirubin(TBIL),γ-glutamyl transpeptidase(γ-GT),superoxide dismutase(T-SOD),malondialdehyde(MDA)and glutathione peroxidase(GSH-Px).The enzyme-linked immunosorbent assay(ELISA)was used to detect the hepatic levels of tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and interleukin-6(IL-6).The relative expressions of TLR-4 and NF-κB in liver tissue were detected by Western blot.HE staining was used to observe the histopathological changes of liver.The results showed that TFC could significantly improve the liver tissue lesion,decrease the liver index and serum contents of AST,ALT,ALP,TBIL,γ-GT and MDA(P<0.05),enhance the activity of T-SOD and GSH-Px(P<0.05),and inhibit the hepatic levels of TNF-α,IL-1β,IL-6,TLR-4 and NF-κB(P<0.05).In summary,TFC had a hepatoprotective effect on mice with acute liver injury induced by CCl₄,and its mechanism may be related to inhibiting the oxidative stress levels,inflammatory response and TLR-4/NF-κB pathway.

To explore the protective effect and mechanism of Qi Wei Jing Gan Ling (QWJGL) on alcoholic liver injury in rats.60 rats were randomly divided into normal group,model group,silymarin group (0.18 g/kg),QWJGL high,medium and low dose group (8,4,2 g/kg),with 10 rats in each group.These groups were given by gavage once a day with 56%vol alcohol at a dose of 10 mL/kg per day,except normal group with distilled water.After 2 h,each drug group were given by gavage for 30 days with QWJGL,normal group and model group to give equal volume distilled water by gavage.After the last intragastric administration fasting for solids and liquids 24 h,reagent kits of ALT,AST,SOD,MDA and GSH-Px were employed for biochemical detection of serum,which isolated from blood sampled by eyeball extirpating.Taking out the liver,spleen and pancreas,and calculate LI,SI and TI.Serum IL-1β,IL-6 and TNF-α were detected by ELISA.CD14 and NF-κB protein levels in rat liver tissues were detected by Western blot.The histopathological changes of liver were observed by HE staining.The results showed that QWJGL reduced the LI of rats with alcoholic liver injury and improved SI and TI (P<0.05).The activity of ALT,AST and the content of MDA were reduced (P<0.05),the activity of SOD and GSH-Px was increased (P<0.05),and the level of TNF-α,IL-6 and IL-1β were reduced(P<0.05).And QWJGL could also inhibit the expression of NF-κB protein and CD14 receptor in liver tissue (P<0.05).It can be seen that the QWJGL has a significant protective effect on alcoholic liver injury,and its protective effect may be related to the inhibition of oxidative stress,inflammatory response,CD14 and NF-κB expressions.

The purpose was to explore the protective effect and mechanism of the extract fraction of the Hypericum japonicum Thunb (HJT) on hepatic fibrosis induced by carbon tetrachloride (CCl₄) in rats.60 male rats were randomly divided into normal group,model group,colchicine (0.12 mg/kg) group and HJT (16 000,8 000,4 000 mg/kg,crude drug dose) groups,with 10 rats in each group.Except for the normal group,other rats were intraperitoneal injection of 40% CCl₄ olive oil mixed solution (1 mL/kg) twice a week for 6 weeks.From the first day of modeling,each administration group was administered by gavage with the corresponding drugs for intervention.Normal group and model group were given the same volume of distilled water once a day.After the last administration,the eyeballs was removed for taking blood and liver tissues were collected.The pathological changes of liver were observed by hematoxylin-eosin staining (HE) and Masson staining.The serum levels of alanine aminotransferase (ALT),aspartate aminotransferase (AST),hyaluronic acid (HA),laminin (LN),procollagetype Ⅲ (PCⅢ) and collage type Ⅳ (Ⅳ-C) were detected by biochemical detection.The levels of superoxide dismutase (SOD),glutathione glutathione peroxidase (GSH-PX),malonaldehyde (MDA),interleukin-1β (IL-1β),interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected by enzyme-linked immunosorbent assay (ELISA).Western blot was used to detect the protein expression of transforming growth factor-β1 (TGF-β1) and α-smooth muscle actin (α-SMA).The results showed that HJT (16 000,8 000,4 000 mg/kg) and colchicine could significantly reduce the activities or contents of ALT,AST,PC-Ⅲ,Ⅳ-C,reduce the level of MDA in liver tissue,increase the activities of SOD and GSH-PX,and reduce the secretions of IL-1β,IL-6 and TNF-α.The results of histological sections showed that the degree of inflammatory necrosis and hepatic fibrosis in liver of each HJT dose group and colchicine group were significantly reduced.The results of the study show that HJT has a significant protective effect on CCl₄-induced hepatic fibrosis,and its mechanism may be related to anti-inflammation,anti-oxidation and inhibition of TGF-β1 protein expression.

To explore the protective effects and its mechanism of Clerodendrum philippinum Schauer var. simplex Mlodenke total flavonoids (CPTF) on acute liver injury induced by carbon tetrachloride (CCl₄) in mice.60 mice were randomly divided into normal group,model group,silymarin group (150 mg/kg),CPTF-high,medium and low dose group (200,100,50 mg/kg).The normal group and model group were given equivoluminal distilled water,and other groups were given the corresponding dose of drugs (25 mL/kg) for 10 days.After 2 h of the last administration,the mice of all groups except the normal group were injected intraperitoneally with 0.1% CCl₄ peanut oil solution (10 mL/kg).16 h later,the blood was taken by removing eye balls,and the liver tissue was collected after killing the mice.The serum contents of alanine aminotransferase (ALT),aspartate aminotransferase (AST),total superoxide dismutase (T-SOD),malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) were measured by biochemical method;the levels of tumor necrosis factor-α (TNF-α),interleukin-1β (IL-1β) and interleukin-6 (IL-6) in liver tissue were detected by enzyme-linked immunosorbent assay (ELISA);janus kinase 2 (JAK2),phosphorylated JAK2 (p-JAK2),signal transducer and activator of transcription 3 (STAT3) and phosphorylated STAT3 (p-STAT3) in liver tissue were detected by Western blot;the histopathological changes of liver were observed by HE staining.The results showed that CPTF could significantly improve the liver tissue lesion,decrease the levels of AST,ALT and MDA in serum (P< 0.05),enhance the activity of T-SOD and GSH-Px (P < 0.05),inhibit the hepatic levels of TNF-α,IL-1β and IL-6 (P< 0.05),and inhibit the expression of p-JAK2 and p-STAT3 (P < 0.05).In summary,CPTF had a protective effect on CCl₄-induced acute liver injury in mice,which could reduce the degree of liver injury,and its mechanism may be related to anti-oxidation,inhibition of inflammation and regulation of JAK2/STAT3 signaling pathway.

To investigate the hepatoprotective activities of Corynoline in the mice model of carbon tetrachloride (CCl₄)-induced liver toxicity.In addition,attempts were made to elucidate the possible mechanism of action.Hepatotoxicity was induced in Kunming mice by a intraperitoneal injection (i.p.) of CCl₄,10 mL/kg body weight,diluted with corn oil at a ratio of 1:500.The corynoline (COR) was administered once a day for 7 days (i.p.) as pretreatment at 10 mg/kg·day.The levels of C-reactive protein (CRP) and tumor necrosis factor-α (TNF-α) were analyzed to determine the inflammation status.The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed by ELISA.Liver ultrastructure was observed via optical microscopy.The protein expression degrees of peroxisome proliferator-activated receptor gamma (PPARγ) and nuclear factor-k gene binding (NF-κB) were assayed by Western blot.CCl₄-induced hepatotoxicity was manifested by an increase in the levels of ALT,AST,CRP and TNF-ɑ.The histopathological examination of liver sections revealed necrosis and inflammatory reactions.The pretreatment with COR decreased levels of ALT,AST,CRP and TNF-ɑ,decreased the protein expression degrees of NFκB,and the protein expression degrees of PPARγ,and normalized the hepatic histo-architecture.This study supported the use of COR against hepatotoxicity,and the hepatoprotective effect was mainly through PPARγ and NF-κB signaling passway.

To study the protection of Rosemary Extract (RE) on acute alcoholic liver injury in mice,and research the mechanism from alcohol metabolism,lipid metabolism,anti-oxidative and anti-inflammation.Mice were randomly divided into control group,model group,Metadoxine Capsules group (MC,200mg/kg·d),RE group (80,160,400 mg/kg·d).The mice were given drugs by gavage 1 time a day and for 30 days.Then,acute alcoholic liver injury model was established by intragastric administration of 56% alcohol (13mg/kg) to the medication and model groups 1h later after the last administration.12h later,the levels of serum ALT,AST,TG,TNF-α,LI-6,IL-10 were detected.The contents of hepatic MDA,SOD,GSH-Px,ADH were determined.The mRNA levels of FAS,ADRP,CYP2E1,PPARα and Caspase3 in liver were also measured by real time PCR.HE straining was performed for observing pathological changes of the liver tissues.Compare with model group,RE can reduce the activity of ADH and contents of ALT,AST,and TG in serum,and shorten the sober time,down regulate Caspase3 expression and relieve acute alcohol liver tissue lesions.The protection mechanism research found thatRE can suppress acute ALD by down-regulatingFAS and ADRP,which can reduce the TG concentration in serum.RE also cure acute ALD by enhancing the activity of SOD,GSH-Px and expressing of PPARα,and down-regulating the expression of CYP2E1,to reduce the level of MDA in liver and relieve oxidative damage.RE can reduce the hepatic inflammation by decreasingTNF-α,IL-6 and increasing IL-10.These results showed thatRE can protect acute alcoholic liver injury by antioxidative,anti-inflammation and regulating lipid metabolism.

Alcoholic hepatic injury is caused by the toxicity of long-term drinking attracts more and more attention in recent years.Increasing studies have shown that a variety of bioactive ingredients in Dendrobium huoshanense C.Z.Tang et S.J.Cheng(DHC) possessed protective effect on alcoholic liver damage.In present study,the protective effect of DHC on alcoholic liver damage was evaluated and the possible underlying mechanism was explored.This study aimed to provide a reliable theoretical basis for the domain of protecting liver for DHC.The hepatoprotective effects of DHC in a mouse model of acute alcohol-induced liver injury were evaluated based on biochemical indicators and antioxidative capacity of serum and liver in 40 d.Severe liver damage caused by 52% ethanol intake with increasing activation of hepatic markers was decreased in the group of mice fed DHC,and the results were confirmed through hematoxylin and eosin staining.Serum biochemical indicators and antioxidative capacity were abnormal by intragastric administration of 52% ethanol,but recovered by DHC.Furthermore,DHC increased the activity of antioxidant enzymes and reduced inflammatory reactions in liver.The experimental results indicate that DHC had preventive and therapeutic effects against acute alcoholinduced liver injury because it could get down the levels of ALT,AST,CRP,TNF-α,MDA,and make up the levels of SOD.DHC treatment significantly decreased the relative levels of NF-κB/p65 and the phosphorylation of p38 MAPK.Therefore,the liver effects of DHC may be attributed to its antioxidant and anti-inflammatory activities,NF-κB/p65 and p38 MAPK may be play important roles in response to acute liver injury and are involved in the inflammatory response and oxidative injury

To study the preventive effect of total flavonoids from Nymphaea candida (NCTF) on carbon tetrachloride (CCl₄) induced liver injury in mice and its mechanism.Sixty mice were equally randomized to six groups:normal group,model group,dimethyl diphenyl bicarboxylate (DDB,150 mg/kg) group and NCTF (50,100,200 mg/kg) group with intragastric administration for seven days.One hour after the last medication,the mice in all groups (except the control group) were intraperitoneal injection of 0.12%CCl₄ soybean oil solution 0.2 mL/10 g.Eight hours later,the eye balls of the mice were removed,blood taken;the mice were then killed,liver and spleen was collected.As compared with the model group,the levels of serum alanine aminotrasferas (ALT),aspartate aminotrasferas (AST),interleukin-6 (IL-6),tumor necrosis factor alpha (TNF-α),liver and spleen index in NCTF group (100,200 mg/kg) as well as liver homogenate malondialde (MDA),and nitric oxide (NO) were notably reduced (P<0.05);the levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were significantly improved (P<0.05).Pretreatment with NCTF at different doses alleviated histopathological changes induced by CCl₄.NCTF had a protective effect on CCl₄ induced acute liver injury in mice,and its mechanism might be related to anti-oxidant and inhibiting of releasing inflammatory cytokines.

In this study,the hepatoprotective and antioxidant activity of Selaginella involventis aqueous extract was evaluated using carbon tetrachloride (CCl₄)induced hepatic damaged mice model.KM mice was randomly divided into 6 groups (n=8),including normal,CCl₄ model,Silymarin control groups and three different dosages (400,200,100 mg/kg) of S.involventis aqueous extract in experimental groups.After oral gavage for 9 days with drug,KM mice were treated with CCl₄ (2 mL/kg) by oral gavage,except for normal group.The results showed that administration of S.involventis aqueous extracts significantly reduced the level of SGOT,SGPT,ALP,Lactic dehydrogenase (LDH),cholesterol and bilirubin when compared to that of hepatotoxin treated mice.More importantly,histopathological data showed that S.involventis aqueous extracts reduced the fatty contents,focal necrosis,congestion in central vein and congestion in sinusoidal spaces in CCl₄-induced hepatic mice.In addition,the in vitro antioxidant assays demonstrated that the IC₅₀ values of T-AOC, LPO,T-SOD and NO radical scavenging activities were increased when compared with the level of vitamin C.All these experimental results suggested that S.involventis aqueous extract may protect hepatic activity through antioxidant activities in CCl₄-induced mice.

The aim of this study was to investigate the protective effects of Piper puberulum(Benth.) Maxim water extract(PTE) on carbon tetrachloride(CCl₄)induced acute liver injury and to explore the possible mechanism.Fifty KM mice were randomly divided into five groups(n=10 in each) including blank group,model group(induced by 0.01 g/kg,0.15% CCl₄ vegetable oil solution),PTE groups(0.5 g/kg and 1.0 g/kg) and positive control group(bifendate 0.15 g/kg).Alanine aminotransferase(ALT),aspartate aminotransferase(AST),malondialdehyde(MDA) content,superoxide dismutase(SOD) activity,tumor necrosis factor(TNF-α),liver wet weight index and HE staining of liver tissue pathological changes were detected in each group.Compared with blank group,the serum ALT,serum AST,liver index,MDA content and serum TNF-α increased significantly(P<0.01),SOD decreased significantly(P<0.01) and hepatic tissue pathology injured significantly(P<0.01) in model group.Compared with model group,the serum ALT decreased significantly in PTE high dose group and positive control group.The serum AST,liver index,MDA content and serum TNF-α decreased significantly(P<0.01 or P<0.05),SOD increased significantly(P<0.01) and hepatic tissue pathology relieved significantly in PTE low dose group,PTE high dose group and positive control group.In conclusion, P.puberulum water extract attenuated the CCl₄-induced acute liver injury and the underlined mechanisms were,at least partly,due to their anti-oxidant actions and inhibitions of TNF-α production.

The aim of this study was to investigate the protective effect ofphytosterolfrom Momordica charantia on paracetamol-induced hepatic damage in mice.Forty-eight mice were randomly divided into normal control group,model group,bifendate group,phytosterol low,medium and high-dose (50,100,and 200 mg/kg) groups,with eight mice in each group.Mice in phytosterol low,medium and high-dose groups were administered with phytosterol for 7 d consecutively.After 7 days,all the mice were then intraperitoneally given paracetamol at a dose of 400 mg/kg.The levels of MDA,SOD,GSH-PX in hepatic tissue and ALT,AST,ALB,TP in serum were measured.Compared with phytosterol groups,in the model group,the level of MDA increased while activities of SOD and GSH-PX decreased in hepatic tissue;the activities of ALT,AST in serum increased significantly while the levels of ALB,TP decreased.Phytosterol had good protective effect on paracetamol-induced hepatic damage in mice.Enhancing defense enzyme activities and eliminating free radical in mice may be the action mechanism of phytosterol.

The aim of this study was to investigate the protective effect of total glycosides from Cistanche salsa on mice alcoholic liver injury according to serum index and histopathology of liver.The three groups of total glycosides of C.salsa were respectively high dose (130 mg/kg),middle dose (100 mg/kg),low dose (65 mg/kg) and bifendate pills (150 mg/kg) was used as positive control.The results showed that ALT,AST and MDA were increased and SOD was decreased in model mice.Besides,the fatty degeneration was also observed in the hepatic cells of model mice.However,high doses of C.salsa total glycosides can effectively improve the liver function.The contents of echinacoside and verbascoside in C.salsa total glycosides were 29.1% by HPLC.In conclusion,total glycosides of C.salsa had a protective effect on mice alcoholic fatty liver injury,and its main active components were echinacoside and verbascoside.

The objective of this study was to explore the extraction and purification technique of flavonoids from Chrysanthemum Morifolium cv.Gongju and to investigate the effect of flavonoids against acute liver injury of mice.The flavonoids were extracted with aqueous ethanol refluxing,purified by column chromatography of polyamide,and flavone powders were obtained by vacuum freeze-drying method.An acute liver injury model of mice induced by carbon tetraehloride was established.The model mice were given bifendate and flavonoids from C.Morifolium cv.Gongju respectively.The GPT/ALT and GOT/AST in blood serum,the activity of SOD and the content of MDA in liver were determined,and the morphology changes of hepatic tissue were observed by HE.The results showed that flavonoids from C.Morifolium cv.Gongju reduced the activity of GPT/ALT and GOT/AST in blood serum of acute liver injury of mice,increased the activity of SOD and decreased the content of MDA in hepatic tissue,and relieved the damage of liver pathological tissue.

The objective of this study was to investigate the effect of alcohol extract of RadixEchinopsison carbon tetrachloride(CCl₄) induced acute liver injuryof mice.The experimentalmodel of acute liver injury was induced by administration of CCl₄ into male mice.The activities of alanine transaminase(ALT),aspartate transaminase(AST)in mice serum were determined.The levels ofsuperoxidedismutase(SOD),MDA and the activity of glutathioneperoxidase(GSH-Px) in liver tissue of mice were also determined.In addition,the liver pathological examination was observed by light microscope.Compared with model groups,the contents of ALT, AST in Radix Echinopsisalcohol extract group was significantly decreased,the content of MDA was also significantly lowered,and the activity of SOD and GSH was significantly improved after preventive treatment with extract of Radix Echinopsis.Hence,it was concluded that Radix Echinopsisalcohol extract has the efficacy of protecting liver from injuryreflected by itsscavenging free radical and antioxidant activities.

Natural taurine widely exists in marine organisms,and it has been reported to exert certain anti-fibrosis activity.Matrix metalloproteinase(MMP-9),Integrin-β1 is closely related to liver fibrosis.In this study,liver cirrhosis rats were treated withdifferent doses of natural taurine(0.3,0.6,1.2 g/kg·d).Fourindices of serum liver fibrosis were analyzed by radioimmunoassay method.MMP-9,Integrin-β1 mRNA expression levels were detected in liver tissue through real-time PCR and related protein levels were determined by Western-blot analysis.The results showed that natural taurine can significantly reduce four indices of serum liver fibrosis in cirrhotic rats.In addition,natural taurinemarkedly reverted the elevated levels of MMP-9,integrin-β1 mRNA and related protein.The 0.6 g/kg·ddosage group showed the highest activity.These results indicated that natural taurine downregulating of MMP-9 and Integrin-β1 expression was closely associated with its protective effects against liver cirrhosis in rats.