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姜黄素和柴胡皂苷 a 抑制大鼠化学诱导的肝炎症和纤维化。

Curcumin and saikosaponin a inhibit chemical-induced liver inflammation and fibrosis in rats.

机构信息

Taipei Medical University, Taiwan.

出版信息

Am J Chin Med. 2010;38(1):99-111. doi: 10.1142/S0192415X10007695.

DOI:10.1142/S0192415X10007695
PMID:20128048
Abstract

Curcumin and saikosaponin A as antioxidants improve antioxidant status. This study investigated the anti-inflammatory and antifibrotic actions of curcumin and saikosaponin A on CCl(4)-induced liver damage. Sprague-Dawley rats were randomly divided into control, CCl(4), CCl(4)+ curcumin (0.005%; CU), CCl(4) + saikosaponin A (0.004%; SS), and CCl(4) + curcumin + saikosaponin A (0.005% + 0.004%; CU + SS) groups. Carbon tetrachloride (40% in olive oil) at a dose of 0.75 ml/kg was injected intraperitoneally once a week. Curcumin and saikosaponin A were supplemented alone or in combination with diet 1 week before CCl(4) injection for 8 weeks. After 8-week supplementation, histopathological results showed hepatic collagen deposition was significantly reduced in the CU and SS groups, and activated nuclear factor-kappa B expression induced by CCl(4) in the liver was significantly inhibited by curcumin and/or saikosaponin A. Hepatic proinflammatory cytokines tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 were significantly inhibited, and anti-inflammatory cytokine interleukin-10 was significantly increased by supplementation with curcumin and/or saikosaponin A. Additionally, curcumin and/or saikosaponin A significantly reduced the increased levels of hepatic transforming growth factor-beta1 and hydroxyproline after CCl(4) treatment. Therefore, supplementation with curcumin and/or saikosaponin A suppress inflammation and fibrogenesis in rats with CCl(4)-induced liver injury. However, the combination has no additive effects on anti-inflammation and antifibrosis.

摘要

姜黄素和柴胡皂苷 A 作为抗氧化剂可改善抗氧化状态。本研究探讨了姜黄素和柴胡皂苷 A 对 CCl4 诱导的肝损伤的抗炎和抗纤维化作用。SD 大鼠随机分为对照组、CCl4 组、CCl4+姜黄素(0.005%;CU)组、CCl4+柴胡皂苷 A(0.004%;SS)组和 CCl4+姜黄素+柴胡皂苷 A(0.005%+0.004%;CU+SS)组。四氯化碳(橄榄油中的 40%)以 0.75ml/kg 的剂量每周腹膜内注射一次。姜黄素和柴胡皂苷 A 在 CCl4 注射前 1 周单独或联合饮食补充,共 8 周。补充 8 周后,组织病理学结果显示,CU 和 SS 组肝胶原沉积明显减少,CCl4 诱导的肝核因子-κB 表达明显受到抑制。姜黄素和/或柴胡皂苷 A 补充可显著抑制肝促炎细胞因子肿瘤坏死因子-α、白细胞介素-1β和白细胞介素-6,显著增加抗炎细胞因子白细胞介素-10。此外,姜黄素和/或柴胡皂苷 A 可显著降低 CCl4 处理后肝转化生长因子-β1 和羟脯氨酸水平的升高。因此,姜黄素和/或柴胡皂苷 A 补充可抑制 CCl4 诱导的肝损伤大鼠的炎症和纤维化。然而,联合用药对抗炎和抗纤维化没有相加作用。

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