Alleviative effects from boswellic acid on acetaminophen-induced hepatic injury
Tóm tắt
Protective effects of boswellic acid (BA) against acetaminophen (APAP)-induced hepatotoxicity in Balb/ cA mice were examined. BA, at 0.05 or 0.1%, was supplied for 4 weeks. Acute liver injury was induced by APAP treatment. Results showed that BA intake increased hepatic BA bioavailability. APAP treatment decreased glutathione (GSH) level, increased reactive oxygen species (ROS) and oxidized glutathione (GSSG) production; and lowered activity and protein expression of glutathione reductase (GR) and heme oxygenase (HO)-1 in liver. BA intake at both doses alleviated subsequent APAP-induced oxidative stress by retaining GSH content, decreasing ROS and GSSG formations, reserving activity and expression of GR and HO-1 in liver, and lowering hepatic cytochrome P450 2E1 activity and expression. APAP treatment enhanced hepatic levels of interleukin-6, tumor necrosis factor-alpha and monocyte chemoattractant protein-1. BA pre-intake diminished APAP-induced release of those inflammatory cytokines and chemokines. APAP upregulated hepatic protein expression of toll-like receptor (TLR)-3, TLR-4, MyD88, nuclear factor kappa B (NF-κB) p50, NF-κB p65 and JNK. BA pre-intake at both doses suppressed the expression of NF-κB p65 and p-JNK, and only at 0.1% down-regulated hepatic TLR-3, TLR-4 and MyD88 expression. APAP led to obvious foci of inflammatory cell infiltration in liver, determined by H&E stain. BA intake at both doses attenuated hepatic inflammatory infiltration. These findings support that boswellic acid is a potent hepatoprotective agent.
Tài liệu tham khảo
Song Z, McClain CJ, Chen T. S-adenosylmethionine protects against acetaminophen-induced hepatotoxicity in mice. Pharmacology 2004; 71: 199–208.
Masubuchi Y, Suda C, Horie T. Involvement of mitochondrial permeability transition in acetaminophen-induced liver injury in mice. J Hepatol 2005; 42: 110–6.
Oz HZ, McClain CJ, Nagasawa HT, Ray MB, de Villiers WJ, Chen TS. Diverse antioxidants protect against acetaminophen hepatotoxicity. J Biochem Molecular Toxicol 2004; 18: 361–8.
Coen M. Metabolic phenotyping applied to pre-clinical and clinical studies of acetaminophen metabolism and hepatotoxicity. Drug Metab Rev 2015; 47: 29–44.
Hsu CC, Lin CC, Liao TS, Yin MC. Protective effect of s-allyl cysteine and s-propyl cysteine on acetaminophen-induced hepatotoxicity in mice. Food Chem Toxicol 2006; 44: 393–7.
Yan SL, Wu ST, Yin MC, Chen HT, Chen HC. Protective effects from carnosine and histidine on acetaminophen-induced liver injury. J Food Sci 2009; 74: 259–65.
Zager RA, Johnson AC, Lund S, Randolph-Habecker J. Toll like receptor (TLR4) shedding and depletion: acute proximal tubular cell responses to hypoxic and toxic injury. Am J Physiol Renal Physiol 2007; 292: 304–12.
Salama M, Elgamal M, Abdelaziz A, Ellithy M, Magdy D, Ali L, et al. Toll-like receptor 4 blocker as potential therapy for acetaminophen- induced organ failure in mice. Exp Ther Med 2015; 10: 241–6.
Cavassani KA, Moreira AP, Habiel D, Ito T, Coelho AL, Allen RM, et al. Toll like receptor 3 plays a critical role in the progression and severity of acetaminophen-induced hepatotoxicity. PLoS One 2013; 8: e65899.
Frank A, Unger M. Analysis of frankincense from various Boswellia species with inhibitory activity on human drug metabolising cyto chrome P450 enzymes using liquid chromatography mass spectrometry after automated on-line extraction. J Chromatogr A 2006; 1112: 255–62.
Ammon HP. Boswellic acids in chronic inflammatory diseases. Planta Med 2006; 72: 1100–16.
Gayathri B, Manjula N, Vinaykumar KS, Lakshmi BS, Balakrishnan A. Pure compound from Boswellia serrata extract exhibits antiinflammatory property in human PBMCs and mouse macrophages through inhibition of TNFalpha, IL-1beta, NO and MAP kinases. Int Immunopharmacol 2007; 7: 473–82.
Yin MC, Lin MC, Mong MC, Lin CY. Bioavailability, distribution, and antioxidative effects of selected triterpenes in mice. J Agric Food Chem 2012; 60: 7697–701.
Lozano-Mena G, Juan ME, García-Granados A, Planas JM. Determination of maslinic acid, a pentacyclic triterpene from olives, in rat plasma by high-performance liquid chromatography. J Agric Food Chem 2012; 60: 10220–5.
Westin J, Lagging LM, Wejstål R, Norkrans G, Dhillon AP. Interobserver study of liver histopathology using the Ishak score in patients with chronic hepatitis C virus infection. Liver 1999; 19: 183–7.
Liu ZX, Kaplowitz N. Role of innate immunity in acetaminopheninduced hepatotoxicity. Expert Opin Drug Metab Toxicol 2006; 2: 493–503.
Farombi EO, Surh YJ. Heme oxygenase-1 as a potential therapeutic target for hepatoprotection. J Biochem Mol Biol 2006; 39: 479–91.
Noh JR, Kim YH, Hwang JH, Choi DH, Kim KS, Oh WK, et al. Sulforaphane protects against acetaminophen-induced hepatotoxicity. Food Chem Toxicol 2015; 80: 193–200.
Manyike PT, Kharasch ED, Kalhorn TF, Slattery JT. Contribution of CYP2E1 and CYP3A to acetaminophen reactive metabolite formation. Clin Pharmacol Ther 2000; 67: 275–82.
Hazai E, Vereczkey L, Monostory K. Reduction of toxic metabolite formation of acetaminophen. Biochem Biophys Res Commun 2002; 291: 1089–94.
Yamaura K, Shimada M, Nakayama N, Ueno K. Protective effects of goldenseal (Hydrastis canadensis L.) on acetaminophen-induced hepatotoxicity through inhibition of CYP2E1 in rats. Pharmacognosy Res 2011; 3: 250–5.
Du K, Williams CD, McGill MR, Xie Y, Farhood A, Vinken M, et al. The gap junction inhibitor 2-aminoethoxy-diphenyl-borate protects against acetaminophen hepatotoxicity by inhibiting cytochrome P450 enzymes and c-jun N-terminal kinase activation. Toxicol Appl Pharmacol 2013; 273: 484–91.
Fouad AA, Jresat I. Hepatoprotective effect of coenzyme Q10 in rats with acetaminophen toxicity. Environ Toxicol Pharmacol 2012; 33: 158–67.
Zimmermann HW, Trautwein C, Tacke F. Functional role of monocytes and macrophages for the inflammatory response in acute liver injury. Front Physiol 2012; 3: 56.
Seki E, Brenner DA, Karin M. A liver full of JNK: signaling in regulation of cell function and disease pathogenesis, and clinical approaches. Gastroenterology 2012; 143: 307–20.
Benias PC, Gopal K, Bodenheimer H, Theise ND. Hepatic expression of toll-like receptors 3, 4, and 9 in primary biliary cirrhosis and chronic hepatitis C. Clin Res Hepatol Gastroenterol 2012; 36: 448–54.
Iimuro Y, Fujimoto J. TLRs, NF-κB, JNK, and liver regeneration. Gastroenterol Res Pract 2010; 2010: 598109.
Djafarzadeh S, Vuda M, Takala J, Ochs M, Jakob SM. Toll-like receptor-3-induced mitochondrial dysfunction in cultured human hepatocytes. Mitochondrion 2011; 11: 83–8.
Zheng Z, Sheng Y, Lu B, Ji L. The therapeutic detoxification of chlorogenic acid against acetaminophen-induced liver injury by ameliorating hepatic inflammation. Chem Biol Interact 2015; 238: 93–101.
Abdel-Tawab M, Werz O, Schubert-Zsilavecz M. Boswellia serrata: an overall assessment of in vitro, preclinical, pharmacokinetic and clinical data. Clin Pharmacokinet 2011; 50: 349–69.