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人参提取物和人参皂苷 Rb1 可减轻大鼠四氯化碳诱导的肝纤维化。

Ginseng extract and ginsenoside Rb1 attenuate carbon tetrachloride-induced liver fibrosis in rats.

机构信息

School of Nutrition and Health Sciences, College of Public Health and Nutrition, Taipei Medical University, Taipei 110, Taiwan.

出版信息

BMC Complement Altern Med. 2014 Oct 25;14:415. doi: 10.1186/1472-6882-14-415.

Abstract

BACKGROUND

Ginsenosides, the major bioactive compounds in ginseng root, have been found to have antioxidant, immunomodulatory and anti-inflammatory activities. This study investigated the effects of ginsenosides on carbon tetrachloride (CCl4)-induced hepatitis and liver fibrosis in rats.

METHODS

Male Sprague-Dawley rats were randomly divided into four groups: control, CCl4, CCl4 + 0.5 g/kg Panax ginseng extract and CCl4 + 0.05 g/kg ginsenoside Rb1 groups. The treated groups were orally given Panax ginseng extract or ginsenoside Rb1 two weeks before the induction of liver injury for successive 9 weeks. Liver injury was induced by intraperitoneally injected with 400 ml/l CCl4 at a dose of 0.75 ml/kg body weight weekly for 7 weeks. The control group was intraperitoneally injected with olive oil.

RESULTS

The pathological results showed that ginsenoside Rb1 decreased hepatic fat deposition (2.65 ± 0.82 vs 3.50 ± 0.75, p <0.05) and Panax ginseng extract lowered hepatic reticular fiber accumulation (1.05 ± 0.44 vs 1.60 ± 0.39, p <0.01) increased by CCl4. Plasma alanine aminotransferase and aspartate aminotransferase activities were increased by CCl4 (p <0.01), and aspartate aminotransferase activity was decreased by Panax ginseng extract at week 9 (p <0.05). Exposure to CCl4 for 7 weeks, the levels of plasma and hepatic triglycerides (p <0.01), hepatic cholesterol (p <0.01), interleukin-1β (p <0.01), prostaglandin E2 (p <0.05), soluble intercellular adhesion molecule-1 (p <0.05), hydroxyproline (p <0.05), matrix metalloproteinase-2 (p <0.05) and tissue inhibitor of metalloproteinase-1 (TIMP-1) (p <0.01) were elevated, however, hepatic interleukin-10 level was lowered (p <0.05). Both Panax ginseng extract and ginsenoside Rb1 decreased plasma and hepatic triglyceride, hepatic prostaglandin E2, hydroxyproline and TIMP-1 levels, and Panax ginseng extract further inhibited interleukin-1β concentrations (p <0.05).

CONCLUSIONS

Panax ginseng extract and ginsenoside Rb1 attenuate plasma aminotransferase activities and liver inflammation to inhibit CCl4-induced liver fibrosis through down-regulation of hepatic prostaglandin E2 and TIMP-1.

摘要

背景

人参根中的主要生物活性化合物人参皂苷具有抗氧化、免疫调节和抗炎作用。本研究探讨了人参皂苷对四氯化碳(CCl4)诱导的大鼠肝炎和肝纤维化的影响。

方法

雄性 Sprague-Dawley 大鼠随机分为四组:对照组、CCl4 组、CCl4+0.5g/kg 人参提取物组和 CCl4+0.05g/kg 人参皂苷 Rb1 组。治疗组在肝损伤诱导前连续 9 周每周口服给予人参提取物或人参皂苷 Rb1。每周一次通过腹腔注射 400ml/l CCl4 0.75ml/kg 体重,连续 7 周诱导肝损伤。对照组腹腔注射橄榄油。

结果

病理结果显示,人参皂苷 Rb1 减少肝脂肪沉积(2.65±0.82 对 3.50±0.75,p<0.05),人参提取物降低肝网状纤维堆积(1.05±0.44 对 1.60±0.39,p<0.01),CCl4 所致升高。CCl4 使血浆丙氨酸氨基转移酶和天冬氨酸氨基转移酶活性升高(p<0.01),人参提取物在第 9 周使天冬氨酸氨基转移酶活性降低(p<0.05)。暴露于 CCl4 7 周后,血浆和肝组织甘油三酯(p<0.01)、胆固醇(p<0.01)、白细胞介素-1β(p<0.01)、前列腺素 E2(p<0.05)、可溶性细胞间黏附分子-1(p<0.05)、羟脯氨酸(p<0.05)、基质金属蛋白酶-2(p<0.05)和组织金属蛋白酶抑制剂-1(TIMP-1)(p<0.01)水平升高,而肝组织白细胞介素-10 水平降低(p<0.05)。人参提取物和人参皂苷 Rb1 均降低了血浆和肝组织甘油三酯、肝组织前列腺素 E2、羟脯氨酸和 TIMP-1 水平,且人参提取物进一步抑制了白细胞介素-1β浓度(p<0.05)。

结论

人参提取物和人参皂苷 Rb1 通过下调肝组织前列腺素 E2 和 TIMP-1,减轻血浆氨基转移酶活性和肝脏炎症,抑制 CCl4 诱导的肝纤维化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f906/4216840/80e35a0bd137/12906_2014_1986_Fig1_HTML.jpg

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