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异烟肼致肝损伤发病机制的研究进展

王玉鹏 鲍婕

王玉鹏, 鲍婕. 异烟肼致肝损伤发病机制的研究进展[J]. 药学实践与服务, 2019, 37(4): 289-293. doi: 10.3969/j.issn.1006-0111.2019.04.001
引用本文: 王玉鹏, 鲍婕. 异烟肼致肝损伤发病机制的研究进展[J]. 药学实践与服务, 2019, 37(4): 289-293. doi: 10.3969/j.issn.1006-0111.2019.04.001
WANG Yupeng, BAO Jie. Research progress on the pathogenesis of isoniazid induced liver injury[J]. Journal of Pharmaceutical Practice and Service, 2019, 37(4): 289-293. doi: 10.3969/j.issn.1006-0111.2019.04.001
Citation: WANG Yupeng, BAO Jie. Research progress on the pathogenesis of isoniazid induced liver injury[J]. Journal of Pharmaceutical Practice and Service, 2019, 37(4): 289-293. doi: 10.3969/j.issn.1006-0111.2019.04.001

异烟肼致肝损伤发病机制的研究进展

doi: 10.3969/j.issn.1006-0111.2019.04.001

Research progress on the pathogenesis of isoniazid induced liver injury

  • 摘要: 异烟肼(isoniazid,INH)是化学预防、治疗结核病的重要药物之一,是四大一线抗结核病药物中至关重要的首选药物。一系列研究表明异烟肼具有肝脏毒性,而其肝损伤机制仍未阐明。对异烟肼肝毒性与其代谢物、线粒体功能障碍、氧化应激、脂质过氧化的关系进行阐述。综述现阶段潜在的异烟肼肝毒性机制研究,为后续深入揭示该方面研究工作提供参考。
  • [1] RAMAPPA V,AITHAL G P.Hepatotoxicity related to anti-tuberculosis drugs:mechanisms and management[J].J Clin Exp Hepatol,2013,3(1):37-49.
    [2] Williams C.Global tuberculosis control:WHO report 2011[J].Austral New Zeal J Publ Health,2012,36(5):497-498.
    [3] DEVARBHAVI H,DIERKHISING R,KREMERS W K. Antituberculosis therapy drug-induced liver injury and acute liver failure[J].Hepatology,2010,52(2):798-799.
    [4] PARK W B,KIM W,LEE K L,et al.Antituberculosis drug-induced liver injury in chronic hepatitis and cirrhosis[J].J Infect,2010,61(4):323-329.
    [5] YEW WW,LEUNG C C.Antituberculosis drugs and hepatotoxicity[J].Am J Respir Crit Care Med,2007,175(8):858.
    [6] WANG P C,PRADHAN K,ZHONG X B,et al.Isoniazid metabolism and hepatotoxicity[J].Acta Pharm Sin B,2016,6(5):384-392.
    [7] METUSHI I G,CAI P,ZHU X,et al.A fresh look at the mechanism of isoniazid-induced hepatotoxicity[J].Clin Pharmacol Ther,2011,89(6):911-914.
    [8] MITCHELL J R,ZIMMERMAN H J,ISHAK K G,et al.Isoniazid liver injury:clinical spectrum,pathology,and probable pathogenesis[J].Ann Intern Med,1976,84(2):181-192.
    [9] INGAWALE D K,MANDLIK S K,NAIK S R.Models ofhepatotoxicity and the underlying cellular,biochemical and immunological mechanism(s):A critical discussion[J].Environ Toxicol Pharmacol,2014,37(1):118-133.
    [10] HASSAN H M,HONGLI G,YOUSEF B A,et al.Hepatotoxicity mechanisms of isoniazid:A mini-review[J].J Appl Toxicol,2015,35(12):1427-1432.
    [11] BALÓ J.Role of hydrazine incarcinogenesis[J].Adv Cancer Res,1979,30:151-164.
    [12] TIMPERIO A M,RINALDUCCI S,ZOLLA L.Hydrazide derivatives produce active oxygen species as hydrazine[J].Bioorg Chem,2005,33(6):459-469.
    [13] PERWITASARI D A,ATTHOBARI J,WILFFERT B. Pharmacogenetics of isoniazid-induced hepatotoxicity[J].Drug Metab Rev,2015,47(2):222-228.
    [14] GARROD S,BOLLARD M E,NICHOLLS A W,et al.Integrated metabonomic analysis of the multiorgan effects of hydrazine toxicity in the rat[J].Chem Res Toxicol,2005,18(2):115-122.
    [15] BANDO K,KUNIMATSU T,JUN S K,et al.GC-MS-based metabolomics reveals mechanism of action for hydrazine induced hepatotoxicity in rats[J].J Appl Toxicol,2011,31(6):524-535.
    [16] OLTHOF E,TOSTMANN A,PETERS W H,et al.Hydrazine-induced liver toxicity is enhanced by glutathione depletion but is not mediated by oxidative stress in HepG2 cells[J].Int J Antimicrob Agents,2009,34(4):385-386.
    [17] BOELSTERLI U A,LEE KK.Mechanisms of isoniazid-induced idiosyncratic liver injury:emerging role of mitochondrial stress[J].J Gastroenterol Hepatol,2014,29(4):678-687.
    [18] PESSAYRE D,MANSOURI A,BERSON A,et al.Mitochondrial involvement in drug-induced liverinjury[J].Handb Exp Pharmacol,2010(196):311-365.
    [19] LEE KK,BOELSTERLI U A.By passing the compromised mitochondrial electron transport with methylene blue alleviates efavirenz/isoniazid-induced oxidant stress and mitochondria-mediated cell death in mouse hepatocytes[J].Redox Biol,2014,2:599-609.
    [20] 张炜.抗结核药物致小鼠肝细胞线粒体损伤的研究[D].河北唐山:华北煤炭医学院,2010:22-26
    [21] BHADAURIA S,SINGH G,SINHA N,et al.Isoniazid induces oxidative stress,mitochondrial dysfunction and apoptosis in HepG2 cells[J].Cell Mol Biol(Noisy-le-grand),2007,53(1):102-114.
    [22] BHADAURIA S,MISHRA R,KANCHAN R,et al.Isoniazid-induced apoptosis in HepG2 cells:generation of oxidative stress and Bcl-2 down-regulation[J].Toxicol Mech Methods,2010,20(5):242-251.
    [23] 郭瑶雪,邓晔,李春,等.异烟肼致线粒体损伤引起药物性肝损伤研究进展[J].中国临床药理学与治疗学,2015,20(3):356-360.
    [24] WU Z R,BAI Z T,SUN Y,et al.Protective effects of the bioactive natural product N-trans-Caffeoyldopamine on hepatotoxicity induced by isoniazid and rifampicin[J].Bioorg Med Chem Lett,2015,25(22):5424-5426.
    [25] CHEN X,XU J,ZHANG C,et al.The protective effects ofursodeoxycholic acid on isoniazid plus rifampicin induced liver injury in mice[J].Eur J Pharmacol,2011,659(1):53-60.
    [26] CEDERBAUM A.Nrf2 and antioxidant Defense against CYP2E1toxicity[J].Expert Opin Drug Metab Toxicol,2009,5(10):1223-1244.
    [27] HASSAN H M,GUO H L,YOUSEF B A,et al.Role of inflammatory and oxidative stress,cytochrome P4502E1,and bile acid disturbance in rat liver injury induced by isoniazid and lipopolysaccharide cotreatment[J].Antimicrob Agents Chemother,2016,60(9):5285-5293.
    [28] CHOWDHURY A,SANTRA A,BHATTACHARJEE K,et al. Mitochondrial oxidative stress and permeability transition inisoniazid and rifampicin induced liver injury in mice[J].J Hepatol,2006,45(1):117-126.
    [29] YUE J,PENG R X,YANG J,et al.CYP2E1 mediatedisoniazid-induced hepatotoxicity in rats[J].Acta Pharmacol Sin,2004,25(5):699-704.
    [30] SHENG Y J,WU G,HE H Y,et al.The association between CYP2E1 polymorphisms and hepatotoxicity due to anti-tuberculosis drugs:A meta-analysis[J].Infect Genet Evol,2014,24:34-40.
    [31] CHEN YY,XUE P,HOU Y Y,et al.Isoniazid suppresses antioxidant response element activities and impairs adipogenesis in mouse and human preadipocytes[J].Toxicol Appl Pharmacol,2013,273(3):435-441.
    [32] SAAD E I,EL-GOWILLY S M,SHERHAA M O,et al.Role of oxidative stress and nitric oxide in the protective effects of alpha-lipoic acid and aminoguanidine against isoniazid-rifampicin-induced hepatotoxicity in rats[J].Food Chem Toxicol,2010,48(7):1869-1875.
    [33] PAL R,RANA S V,VAIPHEI K,et al.Isoniazid-rifampicin induced lipid changes in rats[J].Clin Chim Acta,2008,389(1-2):55-60.
    [34] PALANISAMY N,MANIAN S.Protective effects of Asparagusracemosus on oxidative damage in isoniazid-induced hepatotoxic rats:An in vivo study[J].Toxicol Ind Health,2012,28(3):238-244.
    [35] SHIH T Y,YOUNG T H,LEE H S,et al.Protective effects of kaempferol on isoniazid- and rifampicin-induced hepatotoxicity[J].AAPS J,2013,15(3):753-762.
    [36] DONG Y Z,HUANG J C,LIN X,et al.Hepatoprotective effects of Yulangsan polysaccharide against isoniazid and rifampicin-induced liver injury in mice[J].J Ethnopharmacol,2014,152(1):201-206.
    [37] LI F,LU J,CHENG J,et al.Human PXR modulates hepatotoxicity associated with rifampicin and isoniazid co-therapy[J].Nat Med,2013,19(4):418-420.
    [38] SACHAR M,ANDERSON K E,MA X C.Protoporphyrin IX:the good,the bad,and the ugly[J].J Pharmacol Exp Ther,2016,356(2):267-275.
    [39] FONTANA A O,PIFFARETTI D,MARCHI F,et al.Epithelial growth factor receptor expression influences 5-ALA induced glioblastoma fluorescence[J].J Neurooncol,2017,133(3):497-507.
    [40] LYOUMI S,LEFEBVRE T,KARIM Z,et al.PXR-ALAS1:a key regulatory pathway in liver toxicity induced byisoniazid-rifampicin antituberculosis treatment[J].Clin Res Hepatol Gastroenterol,2013,37(5):439-441.
    [41] SACHAR M,LI F,LIU K,et al.Chronic treatment with isoniazid causes protoporphyrin IX accumulation in mouse liver[J].Chem Res Toxicol,2016,29(8):1293-1297.
    [42] JAMES L,ROBERTS D.Isoniazid hepatotoxicity:progress in understanding the immunologic component[J].Hepatology,2014,59(3):746-748.
    [43] METUSHI I G,UETRECHT J.Isoniazid-induced liver injury and immune response in mice[J].J Immunotoxicol,2014,11(4):383-392.
    [44] SALAZAR-PÓRAMO M,RUBIN R L,GARCÍA-DE LA TORRE I.Systemic lupuserythematosus induced by isoniazid[J].Ann Rheum Dis,1992,51(9):1085-1087.
    [45] UETRECHT J.Immunoallergic drug-induced liver injury in humans[J].Semin Liver Dis,2009,29(4):383-392.
    [46] METUSHI I G,SANDERS C,ACUTE LIVER STUDY GROUP,et al.Detection of anti-isoniazid and anti-cytochrome P450 antibodies in patients with isoniazid-induced liver failure[J].Hepatology,2014,59(3):1084-1093.
    [47] VIGNATI L,TURLIZZI E,MONACI S,et al.An in vitro approach to detect metabolite toxicity due to CYP3A4-dependent bioactivation of xenobiotics[J].Toxicology,2005,216(2-3):154-167.
    [48] 张志华.异烟肼和利福平合用致肝细胞毒性及药物保护机制探讨[D].石家庄:河北医科大学,2009:62-64.
    [49] WEN X,WANG J S,NEUVONEN P J,et al.Isoniazid is a mechanism-based inhibitor of cytochrome P4501A2,2A6,2C19 and 3A4 isoforms in human liver microsomes[J].Eur J Clin Pharmacol,2002,57(11):799-804.
    [50] LIU K,LI F,LU J,et al.Role of CYP3A inisoniazid metabolism in vivo[J].Drug Metab Pharmacokinet,2014,29(2):219-222.
    [51] ORTEGA-ALONSO A,STEPHENS C,LUCENA M I,et al.Case characterization,clinical features and risk factors in drug-induced liver injury[J].Int J Mol Sci,2016,17(5):E714.
    [52] 朱家莲,龚奕,彭文兴.异烟肼/利福平致肝损伤的生物标志物研究进展[J].中国医院药学杂志,2018,38(22):2380-2383.
    [53] TASDUQ S A,PEERZADA K,KOUL S,et al.Biochemical manifestations of anti-tuberculosis drugs induced hepatotoxicity and the effect of silymarin[J].Hepatol Res,2005,31(3):132-135.
    [54] WU Z R,BAI Z T,SUN Y,et al.Protective effects of the bioactive natural product N-trans-Caffeoyldopamine on hepatotoxicity induced by isoniazid and rifampicin[J].Bioorg Med Chem Lett,2015,25(22):5424-5426.
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  • 收稿日期:  2018-12-20
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异烟肼致肝损伤发病机制的研究进展

doi: 10.3969/j.issn.1006-0111.2019.04.001

摘要: 异烟肼(isoniazid,INH)是化学预防、治疗结核病的重要药物之一,是四大一线抗结核病药物中至关重要的首选药物。一系列研究表明异烟肼具有肝脏毒性,而其肝损伤机制仍未阐明。对异烟肼肝毒性与其代谢物、线粒体功能障碍、氧化应激、脂质过氧化的关系进行阐述。综述现阶段潜在的异烟肼肝毒性机制研究,为后续深入揭示该方面研究工作提供参考。

English Abstract

王玉鹏, 鲍婕. 异烟肼致肝损伤发病机制的研究进展[J]. 药学实践与服务, 2019, 37(4): 289-293. doi: 10.3969/j.issn.1006-0111.2019.04.001
引用本文: 王玉鹏, 鲍婕. 异烟肼致肝损伤发病机制的研究进展[J]. 药学实践与服务, 2019, 37(4): 289-293. doi: 10.3969/j.issn.1006-0111.2019.04.001
WANG Yupeng, BAO Jie. Research progress on the pathogenesis of isoniazid induced liver injury[J]. Journal of Pharmaceutical Practice and Service, 2019, 37(4): 289-293. doi: 10.3969/j.issn.1006-0111.2019.04.001
Citation: WANG Yupeng, BAO Jie. Research progress on the pathogenesis of isoniazid induced liver injury[J]. Journal of Pharmaceutical Practice and Service, 2019, 37(4): 289-293. doi: 10.3969/j.issn.1006-0111.2019.04.001
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