Long Lingli, Wang Jingnan, Chen Ningning, Zheng Shuhui, Shi Lanying, Xu Yuxia, Luo Canqiao, Deng Yubin
1 Research Center of Translational Medicine, The First Affiliated Hospital, Sun Yat-Sen University , Guangzhou, China .
2 Department of Spine Surgery, Sun Yat-Sen University , Guangzhou, China .
J Med Food. 2016 Jun;19(6):528-34. doi: 10.1089/jmf.2015.3570. Epub 2016 Feb 12.
The objective of our study was to investigate whether curcumin protects against reserpine-induced gastrointestinal mucosal lesions (GMLs) in rats and to explore the mechanism of curcumin's action. Sprague-Dawley rats were randomly divided into four groups: control group, reserpine-treated group, reserpine treatment group with curcumin at high dose (200 mg/kg), and reserpine treatment group with curcumin at low dose (100 mg/kg). Rats in reserpine-treated group were induced by intraperitoneally administered reserpine (0.5 mg/kg) for 28 days. TUNEL staining and hematoxylin and eosin staining were used to evaluate the apoptotic cells and morphologic changes. In addition, to explore the mechanism of curcumin in protecting GMLs, we used serum of experimental rats to assess the level of vasoactive intestinal peptide (VIP), gastrin, interleukin-6, interleukin-10, tumor necrosis factor-α and interferon-γ by ELISA and radioimmunoassay. The protein levels of NF-κB, p-IκB-α, IκB-α, Bcl-2, Bax, and cleaved-caspase-3 were examined by western blot analysis. Data were analyzed with SPSS 19.0 software package. Curcumin treatment prevented tissue damage and cell death in the reserpine-treated rats and effectively decreased inflammatory response and balanced the expression of VIP and gastrin in the reserpine-treated rats. NF-κB, p-IκB-α, Bax, and cleaved-caspase-3 were increased in the reserpine group, but the curcumin high-dose group inhibited them. Curcumin can target the IκB-α/NF-κB pathway to inhibit inflammatory response and regulate the level of VIP and gastrin in reserpine-induced GML rats.
我们研究的目的是调查姜黄素是否能预防利血平诱导的大鼠胃肠道黏膜损伤(GMLs),并探索姜黄素的作用机制。将Sprague-Dawley大鼠随机分为四组:对照组、利血平处理组、高剂量姜黄素(200mg/kg)利血平处理组和低剂量姜黄素(100mg/kg)利血平处理组。利血平处理组大鼠通过腹腔注射利血平(0.5mg/kg)诱导28天。采用TUNEL染色和苏木精-伊红染色评估凋亡细胞和形态学变化。此外,为了探索姜黄素保护GMLs的机制,我们用实验大鼠的血清通过ELISA和放射免疫分析法评估血管活性肠肽(VIP)、胃泌素、白细胞介素-6、白细胞介素-10、肿瘤坏死因子-α和干扰素-γ的水平。通过蛋白质印迹分析检测NF-κB、p-IκB-α、IκB-α、Bcl-2、Bax和裂解型半胱天冬酶-3的蛋白水平。数据用SPSS 19.0软件包进行分析。姜黄素处理可预防利血平处理大鼠的组织损伤和细胞死亡,并有效降低炎症反应,平衡利血平处理大鼠中VIP和胃泌素的表达。利血平组中NF-κB、p-IκB-α、Bax和裂解型半胱天冬酶-3增加,但姜黄素高剂量组对其有抑制作用。姜黄素可靶向IκB-α/NF-κB途径抑制炎症反应,并调节利血平诱导的GML大鼠中VIP和胃泌素的水平。