绿原酸缓解镉暴露致大鼠肠道损伤

目的：探讨绿原酸缓解镉暴露致大鼠肠道损伤。方法：将32 只大鼠随机分为空白对照组（control， CON）、镉损伤模型组（CdCl2，Cd）、镉损伤模型＋绿原酸治疗组（CdCl2＋chlorogenic acid，Cd＋CGA）、 镉损伤模型＋葵花仁提取物治疗组（CdCl2＋sunflower seed extract，Cd＋SSE）。每日灌胃氯化镉6 mg/kg、绿原 酸50 mg/kg、葵花仁提取物中按绿原酸的量计50 mg/kg，对照组给予相同体积的蒸馏水，连续14 d，定期称量体 质量和采食量。处死后取血液、肝脏、肾脏和肠道。观察肠道黏膜形态，统计黏膜损伤评分，计算绒毛高度， 隐窝深度并测定谷草转氨酶（aspartate aminotransferase，AST）、谷丙转氨酶（alanine aminotransferase，ALT） 活力和血清白蛋白（serum albumin，ALB）水平。结果：绿原酸和葵花仁提取物显著增加镉损伤大鼠体质量，绿 原酸显著增加采食量（P＜0.05）；绿原酸和葵花仁提取物显著缓解由于镉损伤造成的肝脏指数和回肠指数的失 常（P＜0.05），绿原酸显著降低肾脏指数和空肠指数（P＜0.05）；绿原酸和葵花仁提取物显著抑制AST和ALT的 活力（P＜0.05），同时增加镉损伤大鼠肠道绒毛高度和隐窝深度（P＜0.05），形态学观察结果显示绿原酸能有效 地抑制镉造成的黏膜细胞死亡。结论：绿原酸可有效缓解镉造成的肠道损伤。

Chlorogenic Acid Attenuates Cadmium-Induced Intestinal Injury in Rats

Objective: The aim of this work was to investigate the effect of chlorogenic acid (CGA) on cadmium-induced intestinal damage in rats. Methods: A total of 32 rats were randomly divided into normal control (CON) group, cadmiuminduced damage model group (CdCl2, Cd), cadmium damage model + chlorogenic acid treatment group (Cd + CGA) and cadmium damage model + sunflower seed extract treatment group (Cd + SSE). CdCl2 was daily administered by gavage at a dose of 6 mg/kg to the animals, and both chlorogenic acid and SSE (calculated as CGA) at 50 mg/kg. On the other hand, the control group was given an identical volume of distilled water. The administration lasted for 14 d. Body mass and feed intake were regularly recorded during this period. All animals were sacrificed to collect blood, liver, kidney and intestinal tissues. Intestinal mucosal morphology was observed and intestinal mucosal injury score was evaluated. In addition, intestinal villus height and crypt depth were measured and the activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and serum albumin level were determined. Results: CGA and SSE could significantly increase body mass in the rats with cadmium-induced damage and CGA significantly enhanced feed intake (P < 0.05). CGA and SSE could significantly alleviate abnormality of liver index and ileum index in response to cadmium-induced damage (P < 0.05). Moreover, CGA also significantly alleviated abnormality of kidney index and jejunum index (P < 0.05). CGA and SSE significantly inhibited the activities of AST and ALT and increased the intestinal villus height and crypt depth of the rats with cadmium-induced damage (P < 0.05). Morphological observation showed that CGA could effectively inhibit mucosal cell death caused by cadmium. Conclusion: Chlorogenic acid can effectively alleviate cadmium-induced intestinal injury.