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Antiviral therapy is the basic treatment of chronic hepatitis B,and pegylated interferon-α is one of the first-line treatment drugs.At present,several consensuses have been reached on individualized treatment with pegylated interferon-o,which is playing an important role in clinical practice.New clinical demands appear along with the clinical application of pegylated interferon-α.With reference to relevant literature and personal clinical experience,this article elaborates on some knowledge of individualized treatment with pegylated interferon-α for chronic hepatitis B.
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Objective To investigate the efficacy and safety of different optimal therapy strategies for hepatits B e antigen (HBeAg) positive chronic hepatitis B (CHB) patients with suboptimal response to peginterferon-α-2a (peg-IFN-α-2a) at 24 weeks.Methods This open-label,single-center and prospective clinical observational study was conducted in Department of Infectious Diseases at Shanghai Changhai Hospital between January 2009 and December 2011.The cases of HBeAg-positive CHB with suboptimal response to peg-IFN-α-2a at week 24 were enrolled.Based on virological markers and patient preference,patients were treated with either peg-IFN-α-2a add-on adefovir dipivoxil (ADV) or switch-to telbivudine (LdT).Hepatitis B virus (HBV) virological and serological data were collected at week 12,24 and 48 after the initiation of optimal therapy.Adverse reactions were also monitored.Therapeutic efficacy was compared between two groups of patients before and after treatment by x2 test.Kruskall Wallis test and Mann-Whitney test were used for analysis of continuous variables.Results Among 193 HBeAg positive CHB patients treated with interferon,67 had suboptimal response and were enrolled.Forty five cases received peg IFN-α-2a add-on ADV treatment and 22 cases received switch-to LdT treatment.After 48 weeks of optimized therapy,the total tBeAg seroconversion rate was 25.3 ％.The rates of HBeAg loss,HBV DNA negative and alanine aminotransferase normalization were 26.8％,73.1％ and 83.5％,respectively.The peg-IFN-α-2a switch-to LdT strategy had better HBV DNA inhibition efficiency compared with the peg-IFN-α-2a add-on ADV strategy at week 12,24 and 48 (P=0.00,0.00 and 0.01,respectively).However,there was no significant difference of HBV DNA negative rate between two groups at week 48 (x2 =0.01,P=0.89).The obviously intolerable adverse reaction was not reported in two optimized strategy groups.Conclusions The 48-week optimized treatment for HBeAg positive CHB with suboptimal response to peg-IFN-α-2a at week 24 could achieve a higher HBeAg seroconversion rate.The switch-to LdT strategy may have better HBV DNA inhibition efficiency.Both strategies show satisfactory safety and tolerance.
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ObjectiveTo investigate the effects of the imbalance between regulatory T cells (Treg) and T helper 17 cells (Th17) in patients with chronic hepatitis B virus (HBV) infection.MethodsThe serum concentration of Treg/Th17 differentiation-related cytokines in 34 patients with chronic hepatitis B (CHB),20 patients with HBV related acute on chronic liver failure (ACHBLF),and 20 healthy controls (NC) were measured by enzyme-linked immunosorbent assay (ELISA) and proportion of peripheral Th17 and Treg cells were analyzed by flow cytometry.Numeration data was analyzed by Fisher's exact propability method and measurement data was tested by one-factor analysis of variance or Turkey multiple comparison.Results The levels of Th17 differentiation-related cytokines,II-1β (3.97±2.85) pg/mL,IL-6 (12.75±-8.87) pg/mL,and IL-21 (360.0±335.7) pg/ mL in patients with ACHBLF were significantly increased than those in NC,which were (1.87 ±0.94) pg/mL(q=4.559,P＜0.01),(5.28±0.72) pg/mL(q=7.309,P＜0.01) and (46.68±20.17) pg/mL(q=6.946,P＜0.01 ),respectively.The proportion of Th17 increased markedly in patients with ACHBLF than that in NC(q=3.972,P＜0.05).However,compared to NC and patients with ACHBLF,the Treg differentiation-related cytokine,TGF-β,in patients with CHB,increased significantly (q=4.536 and 5.323,respectively; both P＜0.01).And the population of Treg also increased markedly in CHB patients.The level of IL-17A which was the characteristic effector cytokine of Th17 was the highest in patients with ACHBLF.The peripheral Th17 cell proportion was positively correlated with the level of serum total bilirubin in patients with ACHBLF (γ=0.74,P＜0.01).Conclusions Th17 and Treg imbalance including cytokine profiles and cell numbers exists in patients with chronic HBV infection.The Th17 are active in patients with ACHBLF and Treg are active in patients with CHB.
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Objective To investigate expressions of programmed cell death ligand 1 (PD-L1) in hepatic tissues at the different stages of hepatitis B virus ( HBV) infection, and clarify its role in the mechanism of chronic hepatitis B virus infection. Methods The expressions of PD-L1 were detected by immunohistochemistry and computer image quantitative analysis in the hepatic tissues of 65 chronic HBV infected patients and 5 healthy controls. The correlations between PD-L1 expression and inflammatory grading in the hepatic tissues, total bilirubin (TBil), alanine aminotransferase (ALT), aspartate aminotransferase (AST), serum HBV DNA level were analyzed. Results The PD-L1 expressions in hepatic tissues of HBV infection with G0 - G4 inflammatory grades were 3. 07 % ±0.93%, 8.01%±1.49%, 11.60%±2.60%, 18.41%±2.21% and 26. 04% ±3. 41%, respectively,which were all significantly stronger than that in controls (0. 64%±0. 28%). PD-L1 expression was a positively correlated with inflammation grading of hepatitis tissues, TBil, ALT and AST level in serum (r=0. 917, 0. 787, 0. 483, 0. 628; all P<0. 05), and negatively correlated with serum HBV DNA load (r=-0. 620, P<0. 05). Conclusion The upregulated PD-L1 expression may be probably involved in the chronicity of HBV infection.
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Objective To identify the relationship between viral factors and disease progression in patients with acute hepatitis B virus (HBV) infection. Methods Ninety-seven adult patients with acute HBV infection in Shanghai Changhai Hospital were enrolled in this study and followed up for 24 weeks. Epidemiological, biochemical and virological parameters of all patients were collected. HBV S region from sera of 54 patients with acute HBV infection were genotyped using direct nucleotide sequencing. Differences of means between groups were compared by t-test, and frequency between groups was compared by X test. Results The clinical manifestations of all patients were mild and the 83 patients spontaneously developed HBeAg and HBsAg seroconversion. However, 14 patients had a tendency of chronicity, with HBV DNA level higher than patients without chronicity tendency [(6. 17 ±1. 04) 1g copy/mL vs (3. 86±1. 85)1g copy/mL;t = 5. 95, P<0. 01]. Among the 14 patients, 6 obtained HBsAg seroconversion after antiviral therapy and the other 8 developed to be sustained HBV carrier who had not received antiviral therapy. The main genotypes of acute HBV infection were genotypes B and C. There were no statistically significant differences of epidemiological factors and biochemical results between patients with the two genotypes of HBV infection. High viral load at baseline was the risk factor of chronicity tendency. Conclusions The main genotypes of acute HBVinfection in Changhai Hospital in the year from 2003 to 2007 are genotypes B and C. There is no significant relationship between genotype and clinical outcome. While high viral load at baseline is significantly associated with chronicity tendency. Proper antiviral therapy can decrease sustained HBV infection rate.
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Objective To investigate the distribution of genotypes in chronic HBV infection (CHB) and acute HBV infection (AHB) patients in Shanghai. Methods Sixty-two patients with AHB and 73 patients with CHB admitted to ('hanghai Hospital of Shanghai between 2003 and 2007 were studied. Viral genotypes of all the patients were determined by direct gene sequencing.Meanwhile, epidemiological, clinical and biochemical parameters of all patients were collected. Mean values of different groups were compared by t test while frequency was compared by chi square test. Results The major prevalent genotypes in both AHB and CHB patients were genotype B and C (48.4% vs 51.6% in AHB patients and 26.0% vs 74.0% in CHB patients). The proportion of genotype B was higher in AHB patients compared to CHB patients (P= 0.02). Epidemiological factors and clinical outcomes were not statistically different among patients with different viral genotypes. The proportion of genotype C was much higher in CHB patients compared to AHB patients (P=0.006). The main transmission route of AHB was heterosexual interaction which was 18 out of 62 (29.0%), but in CHB patients, it was prenatal transmission which was 38 out of 73 (52.1%). Conclusions In shanghai, the main HBV genotypes in both AHB and CHB patients are genotype B and C. The proportion of genotype B is relatively high in AHB patients while proportion of genotype C is more common in CHB patients. There is no significant relationship between genotypes and the clinical outcomes of AI-IB patients.
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Objective To study the characteristics of lamivudine-resistant mutation associated chronic severe hepatitis B during lamivudine treatment.Methods Twenty-seven patients with lamivudine-resistant mutation associated chronic severe hepatitis B during lamivudine treatment were analyzed retrospectively.YMDD motif mutation was detected by gene chips or DNA sequencing.The pathological features of liver tissues from 8 patients undergoing liver transplantation were analyzed.The X2 test were used to perform the stafistical analysis.Results The YMDD motif mutations of 27 lamivudine-resistant patients were 5 cases of YVDD mutation,2 of YVDD+L180M,13 of YIDD mutation,4 of YIDD+L180M,1 of YVDD+YIDD mutations,2 of YVDD+YIDD+L180M,and there was no single L180 M mutation among patients.Twenty-seven patients were divided into cirrhotic group and noncirrhotic group according to whether they were diagnosed with cirrhosis before treatment.Compared to cirrhotic group,incidence of severe hepatitis was lower,prognosis was better,the age of patients was younger and hepatitis Be antigen(HBeAg)positive rate was higher in noncirrhotic group.There were two types of pathological features of liver tissues from 8 patients,which were active hepatic cirrhosis and massive or submassive hepatic necrosis with liver shrinking significantly.Conclusions Hepatic cirrhosis is a risk factor of lamivudine-resistant mutation associated chronic severe hepatitis B.There may be two mechanisms in lamivudine-resistant mutation associated chronic severe hepatitis B.
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Objective To analyze clinical courses and rescue therapies of adefovir-resistant chronic hepatitis B patients who had lamivudine resistance before and then changed to take adefovir dipivoxil. Methods 15 patients resistant to lamivudine were retrospectively analyzed, who had virological breakthrough after adefovir dipivoxil monotherapy and were treated with rescue therapy.Adefovir-resistant mutations were detected by direct sequencing of the HBV polymerase gene. Results 15 patients with former lamivudine resistance were treated with adefovir dipivoxil monotherapy for a median of 16 months, and 14 patients were found adefovir-resistant mutations at rtA181T/V and(or) rtN236T, only 1 patient was found multi-mutations at rtM204I + rtL180M + rtA181T. Rescue therapies were given to all the 15 patients after drug resistance. Among the 7 patients treated with lamivudine in combination with adefovir for 3 months,whose HBV DNA levels decreased (2.2±0.6)lg copy/mL on average, 5 patients achieved HBV DNA undetectable after 6 months combinative therapy. The HBV DNA levels of the 3 patients treated with entecavir decreased 2.8～3.5 lg copy/mL within 6 months treatment. Conclusion These preliminary data suggest the combination of lamivudine and adeforvir dipivoxil may be an effective rescue therapy for adefovir-resistant patients who have former lamivudine resistance.
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OBJECTIVE: To study the therapeutic effect of Bushen Rougan Recipe (BSRGR) on hepatic fibrosis in rats. METHODS: Forty male Wistar rats were randomly divided into normal control group (n=10), model group (n=15), and BSRGR-treated group (n=15). Rats in the model and BSRGR-treated groups were administered intraperitoneally with 0.5% dimethylnitrosamine (DMN), 10 mg.kg(-1).d(-1), successive 3 days per week for 4 weeks to induce hepatic fibrosis. Then rats in the above 2 groups were given normal saline and BSRGR (10 ml.kg(-1).d(-1), ig) for another 4 weeks, respectively. Rats in the 3 groups were all executed at the end of the 8th week. The serum total bilirubin (TBIL), alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin (A) and globulin (G) were determined and the serum hyaluronic acid (HA), laminin (LN) and collagen IV (IV-C) were measured. RESULTS: The rat model of liver fibrosis was successfully induced by DMN. It was found that the serum TBIL, AST and ALT and the liver fibrosis marks were declined in BSRGR-treated group as compared with those in the model group (P<0.01). The content of total serum protein and the A/G in BSRGR-treated group were both increased as compared with those in the model group (P<0.05). CONCLUSION: BSRGR can be used to treat hepatic fibrosis in rats.
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OBJECTIVE: To study the expression of TIMP-1 and TGF-beta1 mRNA in hepatic fibrosis rats and the therapeutic effects of Bushen Rougan Recipe (BSRGR). METHODS: Hepatic fibrosis was induced in rats by dimethylnitrosamine (DMN). The rats' hepatic tissue was studied by HE staining and Sirius red staining. The rats were divided into normal control group, fibrosis model group and BSRGR treated group (10 g.kg(-1).d(-1), i.g. for 4 weeks). At last, TIMP-1 and TGF-beta1 mRNA were detected by RT-PCR. RESULTS: Pathological study showed that hepatic fibrosis was successfully induced by DMN in rats. The expression quantity of TIMP-1 and TGF-beta1 mRNA were the most in the fibrosis model group, the second in the BSRGR treated group, and the least in the normal control group. CONCLUSION: The expression of TIMP-1 and TGF-beta1 mRNA was increased in the hepatic fibrosis rats, and this is one possible mechanism of hepatic fibrosis. BSRGR can inhibit the advancement of hepatic fibrosis.
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OBJECTIVE: To study the efficacy and safety of Fuzheng Huayu Capsule (FZHY Capsule) against liver fibrosis with chronic hepatitis B. METHODS: Multicentric, randomized, double blinded and paralleled control led trial was conducted on patients (aged between 18 and 65) with liver fibrosis in chronic hepatitis B Indexes observed: (1) hepatic histological changes and HBV markers were observed at 0 and 24th week during the treatment; serological indexes (HA, LN, P-III-P, IV-C) were determined and B ultrasound examination of spleen and liver was taken at 0, 12th, 24th week; liver function (during the period of follow-up, liver function and serological indexes for liver fibrosis were evaluated) were observed at 0, 6th, 12th, 18th, 24th week; (2) indexes for safety: blood and urine routine tests, renal function and ECG were examined. RESULTS: (1) Enrollment and demographic data: There was no significant difference between the trial (110 cases) and control group (106 cases) in demographic feature, vital signs, course of illness, history for drug anaphylaxis, history of previous therapy, liver function, serological indexes for liver fibrosis, liver histological examination (99 cases for test group, 96 cases for control group), HBV markers, and renal function, etc. (2) Histological pathological examination: 93 cases of liver histological examination were taken, of these 50 cases for the trial group and 43 cases for control group which turned out to be at S mean value of 2.33 and 2.11 respectively pretreatment according to criteria for liver fibrosis staging. Post-treatment, the trial showed a significant decrease with S value of 1.80 compared to that of pretreatment; however, there was no significant improvement in control group before and after the treatment with S mean value of 2.14. There was significant difference in reversing rate (decrease at least 1 stage according to criteria for liver fibrosis staging) between the trial (52%) and control (23.3%) after liver biopsy. The trial had a rather good effect on improving inflammatory activity and was superior to control group with a marked decrease of mean value of inflammatory activity and score of inflammation (P<0.05). (3)Serological indexes for liver fibrosis: There was a significant decrease in HA, LN, P-III-P, IV-C content in test group after 12 and 24 weeks' treatment compared to that of pretreatment; the differences of HA, LN, P-III-P, IV-C between 12, 24 weeks' treatment and pretreatment were significantly greater than control group (P<0.01 or 0.05); the effectual was defined as 2 of 4 indexes lowered more than 30% of the baseline, according to this criteria, the trial was 72.7%, while control group 27.4% (P<0.01). (4)Liver function: Obvious improvement of serum Alb, ALT, AST, GGT was seen in 2 groups; compared with control group, marked improvement of GGT and Alb in the trial (P<0.05); the effective rate of serum ALT in the trial group was 72.7%, while control 59.4%. (5)No changes of significant difference between pre- and post-treatment in routine tests for blood and urine, renal function and ECG, etc. There was also no difference in the stable rate of ALT and serological indexes for liver fibrosis between the trial and control group 12 weeks after withdrawal (P<0.05). CONCLUSION: Fuzheng Huayu Capsule has good effect on alleviating liver fibrosis in chronic hepatitis B without any adverse effect and is superior to Heluo Shugan Capsule. Fuzheng Huayu Capsule is a safe and effective medicine for the treatment of liver fibrosis in chronic hepatitis B.
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Objective To analyze the clinical features and mutation patterns of HBV polymerase gene in patients with chronic hepatitis B(CHB) after the emergence of drug-resistance during Lamivudine(LAM) therapy.Methods LAM-resistant mutations were detected by direct sequencing of the HBV polymerase gene in hospitalized patients and outpatients of CHB with LAM-resistance in Changhai Hospital from Dec.2005 to Dec.2007.Clinical features after the emergence of LAM-resistant mutations were retrospectively analyzed.Results Two hundred and fifteen patients with CHB were diagnosed as LAM-resistant.Among them 192 patients were found to have LAM-resistant-associated mutations in the HBV polymerase gene.The mean value of serum HBV DNA was 6.25?1.31(log10copies/ml),the mean value of alanine aminotransferase(ALT) was 75U/L(ranged 19-821 U/L).ALT elevation and hepatitis recrudescence were found in 139 among 192(72.4%) patients.99.0%(190/192) patients had YMDD mutations.Four major mutation patterns of LAM-resistant HBV were identified as rtM204I(33.9%),rtL180M+rtM204V(26.0%),rtL180M+rtM204I(21.9%) and rtV173L+rtL180M+rtM204V(11.5%).The rtM204V mutation was accompanied more frequently by the rtL180M mutation compared with the rtM204I mutation(P0.05).Conclusions YMDD is the major mutation pattern of HBV polymerase gene after emergence of LAM-resistance.The mutation patterns of HBV polymerase gene are possibly not related to the clinical severity of CHB patients during LAM therapy.
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Objective:To construct double copy and x gene deleted HBV expression plasmid and study its expression in Hep3B cell line. Methods:The double copy HBV DNA ( adr Ⅰ) was used to inactivate HBV x gene by inserting mutation and gene recombination. The inserted 55 bp DNA sequence was synthesized artificially; the insertion point was ApaL Ⅰ of x gene area. After recombination, an x gene defected HBV plasmid containing single P, S and C gene was constructed,which can express in mammalian cell line. Another plasmid carrying double copy HBV DNA with normal x gene was constructed as contrast. Both were used to transfect Hep3B cells. Then the cells were screened by G418 and HBV virus in culture medium were isolated and detected by fluorescence quantitative PCR. Results: Plasmids pcDNA3 KN F1F2 and pcDNA3 ES HBV2 were constructed successfully. After cell transfection, the HBV DNA was highly expressed with both plasmids on the 3 rd, 6 th,14th day. Conclusion: The plasmids constructed can express in Hep3B cell line and cause HBV replication; x gene defected HBV gene has no effect on HBV replication in Hep3B cell line.
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Objective: To study the distribution of levofloxacin in the serum and ascites in patients with cirrhosis and to evaluate its efficacy in treatment of patients with spontaneous bacterial peritonitis(SBP). Methods:（1）Concentration of levofloxacin in the serum and ascites was detected with HPLC in 7 patients with cirrhosis at different time (in the serum: 0.5, 1, 1.5, 2 and 12 h;in the ascites:2, 4, 6 and 12 h). （2）The effects of levofloxacin were observed in treatment of 30 patients with SBP. Results:（1） Levofloxacin was determined in serum and ascites of patients with cirrhosis, whose concentration depended on the duration after oral administration. In serum: tmax was 1.5 h and cmax was (3.913±1.388) μg/ml. In ascites: tmax was 6.0 h and cmax was (2.520±1.213) μg/ml. The levels decreased gradually after reaching peak concentration, then stabilized from 12 h.（2）The symptoms and signs were significantly improved in patients with SBP treated with the levofloxacin. Conclusion: After the oral administration, levofloxacin can both distribute in serum and ascites, and it is efficient in the treatment of the patients with SBP.
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Objective To construct an X-gene defect and IFN gene contained HBV expression plasmid and explore its expression effect in HepG2 cell line. Methods By employing pBR322-B-HBV plasmid which contained type adrⅠHBV DNA, we destroyed HBV X-gene by inserting mutation and connected the defect HBV with IFN sequence. After recombination, it was introduced into a mammalian plasmid and was constructed as the objective plasmid. At the same time, two control groups were constructed. One was pcDNA3-ES-HBV2, which contained the full length of HBV DNA. The other was pcDNA3-KN-F1F2, which contained the X-gene defect HBV DNA. Then we transfected HepG2 cells with all the plasmid. After the cells were screened by G418, the X-gene defect and IFN gene contained HBV(KN-F1F2-IFN) and IFN protein from culture medium were detected by fluorescence- quantitative-PCR and ELISA respectively. Results pcDNA3-KN-F1F2-IFN, as the objective plasmid, was constructed successfully; contrary with the control virus, the amounts of both HBV and HBsAg were lower; both IFN mRNA and IFN protein were detected.Conclusions An X-gene defect and IFN gene contained HBV expression plasmid was constructed successfully and it can be expressed in HepG2 cell line.
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Objective:To study the anti-fibrogenetic effect of matrine compound injection and its mechanism. Methods: Experimental liver fibrosis induced by tetrachloride in rats was treated by matrine compound injection. Liver function index, interleukin-1? (IL-1?) and pathological changes in liver tissue were observed in model and therapy groups during the 4th,6th and 9th week. Results:The serum IL-1? levels of model and therapy groups were (25. 51?14. 31) and (10. 49?7. 49) pg/ml in the 4th week, (109. 67?20. 87) and (15. 06?2. 65) pg/ml in the 6th week, and (40. 26?10. 63) and (23. 27?7. 56) pg/ml in the 9th week. The liver function (ALT, AST, TBil) of therapy group was better than that of model group at each stage. Pathological changes indicated that the infiltration of inflammatory cells,the degree of liver cell necrosis and the degree of fi-broplastic proliferation in the therapy group were obviously better than those of the model group. Conclusion : Matrine compound injection has an anti-fibrogenetic action on the liver fibrosis induced by tetrachloride.
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Objective: To prepare the monoclonal antibodies against polycystin 1 intracellular region and to study the distribution and expression of polycystin 1 in kidney tissues. Methods: Using the recombinant fusion protein containing polycystin 1 intracellular region as antigen, the hybrid cells secreting the monoclonal antibodies against polycystin 1 intracellular region were established by hybridoma technique. The distribution and expression of polycystin 1 in polycystic kidney, fetal kidney and adult kidney were investigated by immunohistochemical methods(standard EnVision method) with the monoclonal antibodies. Results: Four cell lines of hybrids steadily secreting the monoclonal antibodies against polycystin 1 intracellular region were established. The antibody titers were 1∶10 6. The 50th generation of these cell lines of hybrids still can secret the monoclonal antibodies and the titers remain similar. Polycystin 1 was weakly expressed in tubules and collecting ducts of normal kidney, the strong staining was seen at tubules of fetal kidney, and very strong staining of cyst lining epithelium of polycystic kidney was observed. Conclusion: The monoclonal antibodies against polycystin 1 intracellular region will be a useful tool in the studies of polycystin 1 structure and function.
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Objective: To study the cellular immunoregulatory effect of Huangqi through intravenous injection in patients with chronic hepatitis B. Methods: In treated groups, light and mild chronic hepatitis B (15 patients in each group) were treated with Huangqi and Ganlixin. In control groups, 10 patients in each group with light and mild chronic hepatitis B were treated with Ganlixin. Normal control group included 10 healthy volunteers. Results: Compared with control group, the level of CD3 +, CD4 + and CD4 + /CD8 + in treatment group increased significantly ( P
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Objective To evaluate the efficacy and safety of adefovir dipivoxil(ADV) monotherapy and ADV lamivudine(LAM) combined therapy for patients with LAM-resistant chronic hepatitis B.Methods 124 chronic hepatitis B patients with LAM-resistant mutations were enrolled in the present study.74 patients were treated with ADV combined with LAM therapy,and other 50 patients subjected to ADV monotherapy.There were no differences between the two groups in patients' baseline characteristics.Sequencing of the HBV polymerase gene was performed to determine LAM and ADV mutations occurred at baseline or during therapy.All patients were monitored with clinical examinations and routine laboratory tests during the therapy.Results The reduced logarithmic values of serum HBV DNA after 12-week and 24-week treatment were 1.99?0.64 and 2.61?0.80 in ADV group,obviously lower compared with those in ADV+LAM group(2.55?0.74 and 3.19?0.82,respectively,P
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To study the effect of heparin on the ConA induced acute liver injury inKunming mice,twenty four mice were randomly divided into groups A,B and C.To the mice in group A, 0 2ml of normal saline (NS) was intravenously administered, while those in group B were given ConA 18mg/kg instead of NS in order to induce severe acute liver injury. Heparin was injected subcutaneously in a dose of 100U per animal at the same time as ConA challenge in group C. Compared with group B, prior injection of heparin in group C significantly decreased the mice death rate and the peak levels of serum ALT within 8h. At the same time, intrasinusoidal congestion and hepatic inflammation were alleviated significantly,and MDA level in liver homogenate was lowered markedly. It suggested that heparin is efficient in protecting the mice from liver injury induced by ConA.