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松属素对硫代乙酰胺诱导的大鼠肝硬化的肝保护作用。

Hepatoprotective effect of pinostrobin against thioacetamide-induced liver cirrhosis in rats.

作者信息

Shareef Suhayla H, Al-Medhtiy Morteta H, Al Rashdi Ahmed S, Aziz Peshawa Y, Abdulla Mahmood A

机构信息

Department of Biology, College of Education, Salahaddin University-Erbil, Erbil, Kurdistan Region, Iraq.

Department of Anatomy and Histology, Faculty of Veterinary Medicine, University of Kufa, Iraq.

出版信息

Saudi J Biol Sci. 2023 Jan;30(1):103506. doi: 10.1016/j.sjbs.2022.103506. Epub 2022 Nov 17.

Abstract

The study assessed the effect of pinostrobin on the histology, immunohistochemistry, and biochemical parameters of thioacetamide (TAA) induced liver cirrhosis in Sprague Dawley rats. The rats were noticeably gavaged with two doses of pinostrobin (30 mg/kg and 60 mg/kg) with TAA and exhibited a substantial decrease in the liver index and hepatocyte propagation with much minor cell injury. These groups meaningfully down-regulated the proliferation of cellular nucleus antigen (PCNA) and alpha-smooth muscle actin (α-SMA). The liver homogenate displayed augmented antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT) activities escorted with reducing in malondialdehyde (MDA) level. The serum level of bilirubin, total protein, albumin, and liver enzymes (ALP, ALT, and AST) returned to normal and was similar to that of normal control and silymarin with TAA-treated groups. pinostrobin-fed groups also decreased the level of Tumor necrosis factor-alpha (TNF-α), Interleukin-6 (IL-6), and increased the level of Interleukin-10 (IL-10). Acute toxicity with a higher dose of 500 mg/kg of pinostrobin did not manifest any toxicological signs in rats. The hepatoprotective effect of pinostrobin could be due to potentially inhibited the progression of liver cirrhosis, down-regulation of PCNA and α-SMA proliferation, prevented oxidation of hepatocytes, improved SOD and CAT enzymes, condensed MDA, repairs of liver biomarkers, reduced cellular inflammation and modulation of inflammatory cytokines.

摘要

该研究评估了松属素对硫代乙酰胺(TAA)诱导的Sprague Dawley大鼠肝硬化的组织学、免疫组织化学和生化参数的影响。给大鼠灌胃两种剂量的松属素(30mg/kg和60mg/kg)加TAA,大鼠的肝脏指数和肝细胞增殖显著降低,细胞损伤轻微得多。这些组显著下调了细胞核抗原(PCNA)和α-平滑肌肌动蛋白(α-SMA)的增殖。肝脏匀浆显示抗氧化酶、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性增强,同时丙二醛(MDA)水平降低。胆红素、总蛋白、白蛋白和肝酶(碱性磷酸酶、谷丙转氨酶和谷草转氨酶)的血清水平恢复正常,与正常对照组和水飞蓟宾加TAA处理组相似。喂食松属素的组也降低了肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)的水平,并提高了白细胞介素-10(IL-10)的水平。500mg/kg高剂量的松属素急性毒性在大鼠中未表现出任何毒理学迹象。松属素的肝保护作用可能是由于潜在地抑制了肝硬化的进展、下调了PCNA和α-SMA增殖、防止了肝细胞氧化、改善了SOD和CAT酶、浓缩了MDA、修复了肝脏生物标志物、减轻了细胞炎症并调节了炎性细胞因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba98/9706172/3fb31efd7fbc/gr1.jpg

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