Liver cirrhosis is a silent disease in humans and is experimentally induced by many drugs and toxins as thioacetamide (TAA) in particular, which is the typical model for experimental induction of hepatic fibrosis. Thus, the objective of the present study was to elucidate the possible protective effects of lactéol® forte (LF) and quercetin dihydrate (QD) against TAA‐induced hepatic damage in male albino rats. Induction of hepatotoxicity was performed by TAA injection (200 mg/kg I/P, twice/ week) in rats. LF (1 × 109 CFU/rat 5 times/week) and QD (50 mg/kg 5 times/week) treated groups were administered concurrently with TAA injection (200 mg/kg I/P, twice/ week). The experimental treatments were conducted for 12 weeks. Hepatotoxicity was evaluated biochemically by measuring alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma‐glutamyl transferase (GGT) in the serum and histopathologically with the scoring of histopathological changes besides histochemical assessment of collagen by Masson's trichrome and immunohistochemical analysis for α‐smooth muscle actin (α‐SMA), Ki67 and caspase‐3 expression in liver sections. Our results indicated that LF and QD attenuated some biochemical changes and histochemical markers in TAA‐mediated hepatotoxicity in rats by amelioration of biochemical markers and collagen, α‐SMA, Ki67 and caspase3 Immunoexpression. Additionally, LF and QD supplementation downregulated the proliferative, necrotic, fibroblastic changes, eosinophilic intranuclear inclusions, hyaline globules and Mallory‐like bodies that were detected histopathologically in the TAA group. In conclusion, LF showed better hepatic protection than QD against TAA‐induced hepatotoxicity in rats by inhibiting inflammatory reactions with the improvement of some serum hepatic transaminases, histopathological picture and immunohistochemical markers.

中文翻译：

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Lactéol® forte 和槲皮素二水合物对雄性白化大鼠硫代乙酰胺诱导的肝硬化的保肝活性

肝硬化是人类的一种无声疾病，由许多药物和毒素在实验上诱发，特别是硫代乙酰胺（TAA），是实验诱发肝纤维化的典型模型。因此，本研究的目的是阐明lactéol® forte (LF) 和槲皮素二水合物(QD) 对TAA 诱导的雄性白化大鼠肝损伤的可能保护作用。通过在大鼠中注射TAA（200 mg/kg I/P，每周两次）来诱导肝毒性。低频（1×109CFU/大鼠5次/周)和QD(50mg/kg 5次/周)治疗组与TAA注射同时施用(200mg/kg I/P，每周两次)。实验治疗进行了12周。通过测量血清中的丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）和γ-谷氨酰转移酶（GGT）来进行生化评估，并通过组织病理学评估，除了通过 Masson 三色法对胶原蛋白进行组织化学评估和α-α-免疫组织化学分析之外，还对组织病理学变化进行评分。肝切片中平滑肌肌动蛋白 (α-SMA)、Ki67 和 caspase-3 的表达。我们的结果表明，LF 和 QD 通过改善生化标记物和胶原蛋白、α-SMA、Ki67 和 caspase3 的免疫表达，减轻了 TAA 介导的大鼠肝毒性中的一些生化变化和组织化学标记物。此外，补充 LF 和 QD 下调了 TAA 组中组织病理学检测到的增殖、坏死、成纤维细胞变化、嗜酸性核内包涵体、透明球和马洛里样小体。总之，对于TAA引起的大鼠肝毒性，LF通过抑制炎症反应并改善一些血清肝转氨酶、组织病理学图像和免疫组化标记物，表现出比QD更好的肝脏保护作用。