Astragalus and Paeoniae radix rubra extract inhibits liver fibrosis by modulating the transforming growth factor‑β/Smad pathway in rats.
Astragalus and Paeoniae radix rubra extract inhibits liver fibrosis by modulating the transforming growth factor‑β/Smad pathway in rats.
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Astagalus和Paeoniae radix Rubra提取物通过调节大鼠的转化生长因子−β/SMAD途径来抑制肝纤维化。
DOI：
10.3892/mmr.2014.2868
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发表时间：
2015-02
影响因子：
3.4
通讯作者：
Qiu G
中科院分区：
文献类型：
--
作者：
Huang W;Li L;Tian X;Yan J;Yang X;Wang X;Liao G;Qiu G
黄芪和赤芍提取物（APE）对小鼠肝纤维化具有保护作用。本研究旨在探讨APE对ccl4诱导大鼠肝纤维化的保护作用。雄性Sprague-Dawley大鼠经腹腔注射50% CCl4，每周2次，连续8周诱导肝纤维化。测定肝纤维化大鼠脏器系数、血清天冬氨酸转氨酶（AST）、丙氨酸转氨酶（ALT）、十六烯酸（HA）、层粘连蛋白（LN）、III型前胶原（PCIII）、羟脯氨酸（Hyp）、谷胱甘肽（GSH-Px）、丙二醛（MDA）、超氧化物歧化酶（SOD）、转化生长因子β1 （TGF-β1）水平。用苏木精-伊红和马松三色染色法观察病变肝脏的组织病理学变化。western blot法观察纤维化肝组织中转化生长因子-β/Smad通路蛋白、α-平滑肌肌动蛋白（α-SMA）、I型胶原和III型胶原的表达。本研究观察到，给药（2.6 g/kg和5.2 g/kg）的大鼠血清AST、ALT、HA、LN、PCIII和Hyp水平显著降低，表明APE具有显著的肝保护作用。此外，2.6和5.2 g/kg的APE可抑制肝组织中GSH-Px和SOD的消耗以及MDA的积累。ccl4诱导的肝纤维化的病理评估显示，用APE（2.6和5.2 g/kg）处理的大鼠肝损伤和肝纤维化的发生显著减少。此外，APE（2.6和5.2 g/kg）降低了TGF-β1、α-SMA、I型胶原和III型胶原表达的升高，抑制了Smad2/3的磷酸化，提高了TGF-β1抑制剂Smad7的表达。这些结果表明，APE可能对肝损伤有保护作用，并抑制ccl4诱导的肝纤维化的进展。APE的作用机制可能是通过清除自由基、降低TGF-β1水平和阻断TGF-β/Smad信号通路来实现的。
It has been previously demonstrated that Astragalus and Paeoniae radix rubra extract (APE) had a protective effect against liver fibrosis in mice. The present study aimed to investigate the hepatoprotective effect of APE on CCl4-induced hepatic fibrosis in rats. Liver fibrosis was induced in male Sprague-Dawley rats by intraperitoneal injection of 50% CCl4 twice a week for eight weeks. Organ coefficients, serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), hexadecenoic acid (HA), laminin (LN), procollagen type III (PCIII), hydroxyproline (Hyp), glutathione (GSH-Px), malondialdehyde (MDA), superoxide dismutase (SOD) and transforming growth factor β1 (TGF-β1) levels were measured in rats with hepatic fibrosis. Histopathological changes in affected livers were studied using hematoxylin-eosin and Masson’s trichrome staining. The expression of transforming growth factor-β/Smad pathway proteins, α-smooth muscle actin (α-SMA), collagen I and collagen III was observed in fibrotic livers using western blot analysis. The present study observed significant reductions in serum levels of AST, ALT, HA, LN, PCIII and Hyp in APE-treated (2.6 and 5.2 g/kg) rats, indicating the significant hepatoprotective effects of APE. Furthermore, the depletion of GSH-Px and SOD, in addition to the accumulation of MDA in liver tissue was suppressed by APE (2.6 and 5.2 g/kg). Pathological assessment of CCl4-induced fibrotic livers revealed a significant reduction of liver injury and development of hepatic fibrosis in rats treated with APE (2.6 and 5.2 g/kg). Moreover, APE (2.6 and 5.2 g/kg) decreased the elevation of TGF-β1, α-SMA, collagen I and collagen III expression, inhibited Smad2/3 phosphorylation as well as elevated the expression of the TGF-β1 inhibitor Smad7. These results suggested that APE may protect against liver damage and inhibit the progression of CCl4-induced hepatic fibrosis. The mechanism of action of APE is hypothesized to proceed via scavenging free radicals, decreasing TGF-β1 levels and blocking of the TGF-β/Smad signaling pathway.
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影响因子：
2.4
作者：
Mera K;Uto H;Mawatari S;Ido A;Yoshimine Y;Nosaki T;Oda K;Tabu K;Kumagai K;Tamai T;Moriuchi A;Oketani M;Shimada Y;Hidaka M;Eguchi S;Tsubouchi H
通讯作者：
Tsubouchi H
DOI：
10.1111/j.1440-1746.2006.04447.x
发表时间：
2006-09-01
影响因子：
4.1
作者：
Kaneda, Hiroyuki;Hashimoto, Etsuko;Shiratori, Keiko
通讯作者：
Shiratori, Keiko
影响因子：
3.3
作者：
Koh, YH;Park, YS;Taniguchi, N
通讯作者：
Taniguchi, N
DOI：
10.1016/0885-4505(88)90102-8
发表时间：
1988-08-01
期刊：
BIOCHEMICAL MEDICINE AND METABOLIC BIOLOGY
影响因子：
--
作者：
NADKARNI, GD;DSOUZA, NB
通讯作者：
DSOUZA, NB
DOI：
10.1186/1755-1536-5-s1-s17
发表时间：
2012
期刊：
Fibrogenesis & tissue repair
影响因子：
--
作者：
Brenner DA;Kisseleva T;Scholten D;Paik YH;Iwaisako K;Inokuchi S;Schnabl B;Seki E;De Minicis S;Oesterreicher C;Taura K
通讯作者：
Taura K