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Taxifolin, Extracted from Waste Larix olgensis Roots, Attenuates CCl4-Induced Liver Fibrosis by Regulating the PI3K/AKT/mTOR and TGF-β1/Smads Signaling Pathways
Drug Design, Development and Therapy ( IF 4.7 ) Pub Date : 2021-02-26 , DOI: 10.2147/dddt.s281369 Xinglong Liu 1 , Wencong Liu 1, 2 , Chuanbo Ding 1 , Yingchun Zhao 1 , Xueyan Chen 1 , Dong Ling 1 , Yinan Zheng 1 , Zhiqiang Cheng 3
Drug Design, Development and Therapy ( IF 4.7 ) Pub Date : 2021-02-26 , DOI: 10.2147/dddt.s281369 Xinglong Liu 1 , Wencong Liu 1, 2 , Chuanbo Ding 1 , Yingchun Zhao 1 , Xueyan Chen 1 , Dong Ling 1 , Yinan Zheng 1 , Zhiqiang Cheng 3
Affiliation
Purpose: Taxifolin is a kind of dihydroflavone and is usually used as a food additive and health food for its antioxidant, anti-inflammatory, and anti-tumor activities. The purpose of this research is to probe into the hepatoprotective activity and the molecular mechanism of taxifolin.
Materials and Methods: The liver fibrosis model was established by intraperitoneal injection of 5 mL/kg body weight of CCl4 (20% CCl4 peanut oil solution), and taxifolin was dissolved with 0.9% physiological saline and administered intragastrically to mice.
Results: The results indicated that CCl4-induced significantly increased the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in mice. Histopathological examination showed severe hepatocyte necrosis and hepatic tissue lesion. Immunohistochemical staining and rt-PCR analysis demonstrated that the expressions of inducible nitric oxide synthetase (iNOS), cyclooxygenase-2 (COX-2), IL-1β, IL-6, and TNF-α were increased. These changes were significantly reversed when treated with taxifolin. In addition, TUNEL staining and Bcl-2/Bax pathway confirmed that taxifolin significantly inhibited hepatocyte apoptosis. Besides, the research confirmed that taxifolin also inhibited the activation of hepatic stellate cells and the production of extracellular matrix (ECM) by regulating PI3K/AKT/mTOR and TGF-β 1/Smads pathways.
Conclusion: Taxifolin inhibited inflammation, and attenuated CCl4-induced oxidative stress and cell apoptosis by regulating PI3K/AKT/mTOR and TGF-β 1/Smads pathways, which might in part contributed to taxifolin anti-hepatic fibrosis, further demonstrating that taxifolin may be an efficient hepatoprotective agent.
Keywords: taxifolin, liver fibrosis, PI3K/AKT/mTOR pathway, TGF-β 1/Smads, inflammation, apoptosis
中文翻译：
从废弃落叶松根中提取的紫杉叶素通过调节 PI3K/AKT/mTOR 和 TGF-β1/Smads 信号通路减轻 CCl4 诱导的肝纤维化
用途：紫杉叶素是一种二氢黄酮类化合物，具有抗氧化、抗炎、抗肿瘤等活性，常被用作食品添加剂和保健食品。本研究旨在探讨紫杉叶素的保肝活性及其分子机制。
材料与方法：腹腔注射5 mL/kg体重的CCl 4（20% CCl 4花生油溶液）建立肝纤维化模型，紫杉叶素用0.9%生理盐水溶解后灌胃给药。
结果：结果表明，CCl 4-诱导小鼠血清丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）显着升高。组织病理学检查显示有严重的肝细胞坏死和肝组织病变。免疫组织化学染色和 rt-PCR 分析表明诱导型一氧化氮合成酶 (iNOS)、环氧合酶-2 (COX-2)、IL-1β、IL-6 和 TNF-α 的表达增加。当用紫杉叶素治疗时，这些变化显着逆转。此外，TUNEL 染色和 Bcl-2/Bax 通路证实紫杉叶素显着抑制肝细胞凋亡。此外，研究证实紫杉叶素还通过调节PI3K/AKT/mTOR和TGF-β1/Smads通路抑制肝星状细胞的活化和细胞外基质(ECM)的产生。
结论：紫杉叶素通过调节 PI3K/AKT/mTOR 和 TGF-β 1/Smads 通路抑制炎症，减弱 CCl 4诱导的氧化应激和细胞凋亡，这可能部分有助于紫杉叶素抗肝纤维化，进一步证明紫杉叶素可能是一种高效的保肝剂。
关键词：紫杉叶素，肝纤维化，PI3K/AKT/mTOR通路，TGF-β1/Smads，炎症，细胞凋亡
更新日期：2021-04-20
Materials and Methods: The liver fibrosis model was established by intraperitoneal injection of 5 mL/kg body weight of CCl4 (20% CCl4 peanut oil solution), and taxifolin was dissolved with 0.9% physiological saline and administered intragastrically to mice.
Results: The results indicated that CCl4-induced significantly increased the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in mice. Histopathological examination showed severe hepatocyte necrosis and hepatic tissue lesion. Immunohistochemical staining and rt-PCR analysis demonstrated that the expressions of inducible nitric oxide synthetase (iNOS), cyclooxygenase-2 (COX-2), IL-1β, IL-6, and TNF-α were increased. These changes were significantly reversed when treated with taxifolin. In addition, TUNEL staining and Bcl-2/Bax pathway confirmed that taxifolin significantly inhibited hepatocyte apoptosis. Besides, the research confirmed that taxifolin also inhibited the activation of hepatic stellate cells and the production of extracellular matrix (ECM) by regulating PI3K/AKT/mTOR and TGF-β 1/Smads pathways.
Conclusion: Taxifolin inhibited inflammation, and attenuated CCl4-induced oxidative stress and cell apoptosis by regulating PI3K/AKT/mTOR and TGF-β 1/Smads pathways, which might in part contributed to taxifolin anti-hepatic fibrosis, further demonstrating that taxifolin may be an efficient hepatoprotective agent.
Keywords: taxifolin, liver fibrosis, PI3K/AKT/mTOR pathway, TGF-β 1/Smads, inflammation, apoptosis
中文翻译：
从废弃落叶松根中提取的紫杉叶素通过调节 PI3K/AKT/mTOR 和 TGF-β1/Smads 信号通路减轻 CCl4 诱导的肝纤维化
用途：紫杉叶素是一种二氢黄酮类化合物，具有抗氧化、抗炎、抗肿瘤等活性，常被用作食品添加剂和保健食品。本研究旨在探讨紫杉叶素的保肝活性及其分子机制。
材料与方法：腹腔注射5 mL/kg体重的CCl 4（20% CCl 4花生油溶液）建立肝纤维化模型，紫杉叶素用0.9%生理盐水溶解后灌胃给药。
结果：结果表明，CCl 4-诱导小鼠血清丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）显着升高。组织病理学检查显示有严重的肝细胞坏死和肝组织病变。免疫组织化学染色和 rt-PCR 分析表明诱导型一氧化氮合成酶 (iNOS)、环氧合酶-2 (COX-2)、IL-1β、IL-6 和 TNF-α 的表达增加。当用紫杉叶素治疗时，这些变化显着逆转。此外，TUNEL 染色和 Bcl-2/Bax 通路证实紫杉叶素显着抑制肝细胞凋亡。此外，研究证实紫杉叶素还通过调节PI3K/AKT/mTOR和TGF-β1/Smads通路抑制肝星状细胞的活化和细胞外基质(ECM)的产生。
结论：紫杉叶素通过调节 PI3K/AKT/mTOR 和 TGF-β 1/Smads 通路抑制炎症，减弱 CCl 4诱导的氧化应激和细胞凋亡，这可能部分有助于紫杉叶素抗肝纤维化，进一步证明紫杉叶素可能是一种高效的保肝剂。
关键词：紫杉叶素，肝纤维化，PI3K/AKT/mTOR通路，TGF-β1/Smads，炎症，细胞凋亡
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