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首页> 外文期刊>Journal of medicinal food >Curcumin Ameliorates Reserpine-Induced Gastrointestinal Mucosal Lesions Through Inhibiting I kappa B-alpha/NF-kappa B Pathway and Regulating Expression of Vasoactive Intestinal Peptide and Gastrin in Rats
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Curcumin Ameliorates Reserpine-Induced Gastrointestinal Mucosal Lesions Through Inhibiting I kappa B-alpha/NF-kappa B Pathway and Regulating Expression of Vasoactive Intestinal Peptide and Gastrin in Rats

机译:姜黄素通过抑制大鼠IκB-α/NF-κB通路并调节大鼠血管活性肠肽和胃泌素的表达来减轻利血平诱导的胃肠道粘膜病变

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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-alpha and interferon-gamma by ELISA and radioimmunoassay. The protein levels of NF-kappa B, p-I kappa B-alpha, I kappa B-alpha, 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-kappa B, p-I kappa B-alpha, Bax, and cleaved-caspase-3 were increased in the reserpine group, but the curcumin high-dose group inhibited them. Curcumin can target the I kappa B-alpha/NF-kappa B pathway to inhibit inflammatory response and regulate the level of VIP and gastrin in reserpine-induced GML rats.
机译:我们研究的目的是研究姜黄素是否能预防利血平诱导的大鼠胃肠道粘膜损伤(GML),并探讨姜黄素的作用机理。将Sprague-Dawley大鼠随机分为四组:对照组,利血平治疗组,高剂量姜黄素(200 mg / kg)利血平治疗组和低剂量姜黄素(100 mg / kg)利血平治疗组。利血平治疗组的大鼠通过腹膜内给予利血平(0.5 mg / kg)诱导28天。 TUNEL染色,苏木精和曙红染色用于评估凋亡细胞和形态学变化。此外,为探讨姜黄素保护GML的机制,我们使用实验大鼠血清评估血管活性肠肽(VIP),胃泌素,白介素-6,白介素-10,肿瘤坏死因子-α和干扰素-γ的水平。通过ELISA和放射免疫测定。通过蛋白质印迹分析检查了NF-κB,p-1κB-α,IκB-α,Bcl-2,Bax和裂解的胱天蛋白酶-3的蛋白水平。使用SPSS 19.0软件包分析数据。姜黄素治疗预防了利血平治疗大鼠的组织损伤和细胞死亡,并有效降低了炎症反应并平衡了利血平治疗大鼠的VIP和胃泌素表达。利血平组中NF-κB,p-1κB-α,Bax和裂解的caspase-3增加,但是姜黄素高剂量组抑制了它们。姜黄素可以靶向IκB/NFκB通路,以抑制炎症反应并调节利血平诱导的GML大鼠的VIP和胃泌素水平。

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