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Hydroxysafflor yellow A protects against thioacetamide-induced liver fibrosis in rats via suppressing proinflammatory/fibrogenic mediators and promoting hepatic stellate cell senescence and apoptosis

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Asian Pacific Journal of Tropical Biomedicine 2023年第8期13卷 348-358页

作者： Sayed H.Seif el-Din Olfat A.Hammam Shahira m.Ezzat Samira Saleh marwa m.safar Walaa H.El-maadawy Naglaa m.El-Lakkany Pharmacology Department Theodor Bilharz Research InstituteWarak El-HadarImbaba P.O.Box 30Giza 12411Egypt Pathology Department Theodor Bilharz Research InstituteWarak El-HadarImbaba P.O.Box 30Giza 12411Egypt Pharmacognosy Department Faculty of PharmacyCairo UniversityCairo 11562Egypt Pharmacognosy Department Faculty of PharmacyOctober University for Modern Sciences and ArtsGizaEgypt Pharmacology and Toxicology Department Faculty of PharmacyCairo UniversityCairo 11562Egypt Pharmacology and Biochemistry Department Faculty of PharmacyThe British University in EgyptCairoEgypt

Objective:To evaluate the effect of hydroxysafflor yellow A(HSYA)on thioacetamide-induced liver ***:Thioacetamide was administered to rats intraperitoneally in doses of 200 mg/kg twice a week for 12 ***-intoxicated rats were given silymarin(50 mg/kg)or HSYA(5 mg/kg)orally every day for 8 *** enzymes,fibrosis markers,histological changes as well as immunohistochemistry of TNF-α,IL-6,p21,α-SmA,and caspase-3 were *** effect of HSYA on HSC-T6 activation/proliferation and apoptosis was also determined in ***:HSYA decreased liver enzymes,TNF-α,IL-6,and p21 expressions,hepatic PDGF-B,TImP-1,TGF-β1,and hydroxyproline levels,as well as fibrosis score(S2 vs.S4)compared to the thioacetamide *** also downregulatedα-SmA while increasing caspase-3 ***,at 500μg/mL,HSYA had only a slightly suppressive effect on HSC proliferation,with a 9.5%***,it significantly reduced TGF-β1,inhibitedα-SmA expression,induced caspase-3 expression,and promoted cell ***:HSYA may be a potential therapeutic agent for delaying and reversing the progression of liver *** research on HSYA at higher doses and for a longer period is warranted.

关键词： Hydroxysafflor yellow A Thioacetamide Hepatic stellate cells Inflammatory markers Liver fibrosis p21 α-SmA Apoptosis

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Rosmarinic acid attenuates hepatic fibrogenesis via suppression of hepatic stellate cell activation/proliferation and induction of apoptosis

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Asian Pacific Journal of Tropical medicine 2017年第5期10卷 423-432页

作者： Naglaa m.El-Lakkany Walaa H.El-maadawy Sayed H.Seif el-Din Olfat A.Hammam Salwa H.mohamed Shahira m.Ezzat marwa m.safar Samira Saleh Department of Pharmacology Theodor Bilharz Research InstituteWarak El-HadarImbaba P.O.Box 30Giza 12411Egypt Department of Pathology Theodor Bilharz Research InstituteWarak El-HadarImbaba P.O.Box 30Giza 12411Egypt Department of Immunology Theodor Bilharz Research InstituteWarak El-HadarImbaba P.O.Box 30Giza 12411Egypt Department of Pharmacognosy Faculty of PharmacyCairo UniversityCairo 11562Egypt Department of Pharmacology and Toxicology Faculty of PharmacyCairo UniversityCairo 11562Egypt

Objective:To investigate the antifibrotic role of rosmarinic acid(RA),a natural polyphenolic compound,on HSCs activation/proliferation and apoptosis in vitro and in vivo. methods:The impact of RA on stellate cell line(HSC-T6) proliferation,activation and apoptosis was assessed along with its safety on primary hepatocytes. In vivo,rats were divided into:(i) normal;(ii) thioacetamide(TAA)-intoxicated rats for 12 weeks;(iii) TAA+silymarin or(iv) TAA+RA. At the end of experiment,liver functions,oxidative stress,inflammatory and profibrogenic markers,tissue inhibitor metalloproteinases type-1(TImP-1) and hydroxyproline(HP) levels were evaluated. Additionally,liver histopathology and immunohistochemical examinations of alpha-smooth muscle actin(α-SmA),caspase-3 and proliferation cellular nuclear antigen(PCNA) were determined. Results:RA exhibited anti-proliferative effects on cultured HSCs in a time and concentration dependent manner showing an IC50 of 276 μg/mL and 171 μg/mL for 24 h and 48 h,respectively,with morphological reversion of activated stellate cell morphology to quiescent form. It significantly improved ALT,AST,oxidative stress markers and reduced TImP-1,HP levels,inflammatory markers and fibrosis score(S1 vs S4). Furthermore,reduction in α-SmA plus elevation in caspase-3 expressions of HSCs in vitro and in vivo associated with an inhibition in proliferation of damaged hepatocytes were recorded. Conclusions:RA impeded the progression of liver fibrosis through inhibition of HSCs activation/proliferation and induction of apoptosis with preservation of hepatic architecture.

关键词： Hepatic fibrosis Hepatic stellate cells Rosmarinic acid Apoptosis Proliferation Profibrogenic markers

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