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姜黄素-半乳甘露聚糖复合物通过抑制炎症和氧化应激对乙酸诱导的实验模型的抗溃疡作用。

Anti-Ulcerative Effect of Curcumin-Galactomannoside Complex on Acetic Acid-Induced Experimental Model by Inhibiting Inflammation and Oxidative Stress.

机构信息

Department of Biochemistry, St. Thomas College, Pala, Kottayam, Kerala, 686574, India.

R & D Centre, Akay Flavours & Aromatics Pvt Ltd, Cochin, India.

出版信息

Inflammation. 2020 Aug;43(4):1411-1422. doi: 10.1007/s10753-020-01218-9.

Abstract

Ulcerative colitis (UC) is a chronic inflammatory bowel disease that affects the mucosa and submucosa of colon. The pathogenesis of ulcerative colitis (UC) is related to reduced antioxidant capacity and increased inflammatory processes. Reactive oxygen metabolites are the potent inflammatory mediators that may be involved in tissue injury in inflammatory bowel disease. Conventional drug therapies for UC come with a myriad of side effects which further raise the need for natural bioactive agents. Curcumin has proven to be beneficial in the prevention and treatment of a number of inflammatory diseases, but due its poor bioavailability, the therapeutic applications are limited. Thus, to enhance its bioavailability, a new formulation - curcumin-galactomannoside (CGM)- was made by complexing curcumin with galactomannans derived from fenugreek. The present study aims to evaluate the effects of CGM on experimental UC model. Adult male Wistar rats were divided into 5 groups: normal control rats (NC); ulcerative colitis control rats (UC); UC + sulfasalazine (SS) treated; UC + curcumin (CM) treated; and UC + CGM supplemented for 21 days. The colonic mucosal injury was assessed by macroscopic and histological examination, along with evaluation of antioxidant status, inflammatory mediators, and gene expressions. Administration of CGM significantly enhanced antioxidant activities and decreased the level of inflammatory mediators and also suppressed the expression of inflammatory markers as compared with other groups. In conclusion, findings from these results reveal that CGM exerts marked curative effects on acute experimental colitis, possibly by regulating the antioxidant status and modulating inflammatory cascade.

摘要

溃疡性结肠炎(UC)是一种慢性炎症性肠病,影响结肠的黏膜和黏膜下层。溃疡性结肠炎(UC)的发病机制与抗氧化能力降低和炎症过程增加有关。活性氧代谢物是潜在的炎症介质,可能参与炎症性肠病中的组织损伤。UC 的传统药物治疗方法有很多副作用,这进一步增加了对天然生物活性物质的需求。姜黄素已被证明对许多炎症性疾病的预防和治疗有益,但由于其生物利用度差,治疗应用受到限制。因此,为了提高其生物利用度,通过将姜黄素与来源于葫芦巴的半乳甘露聚糖复合,制备了一种新的制剂 - 姜黄素-半乳甘露聚糖(CGM)。本研究旨在评估 CGM 对实验性 UC 模型的影响。成年雄性 Wistar 大鼠分为 5 组:正常对照组(NC);溃疡性结肠炎对照组(UC);溃疡性结肠炎+柳氮磺胺吡啶(SS)治疗组;溃疡性结肠炎+姜黄素(CM)治疗组;溃疡性结肠炎+CGM 补充治疗组,共 21 天。通过宏观和组织学检查评估结肠黏膜损伤,并评估抗氧化状态、炎症介质和基因表达。与其他组相比,CGM 的给药显著增强了抗氧化活性,降低了炎症介质水平,并抑制了炎症标志物的表达。总之,这些结果表明,CGM 对急性实验性结肠炎具有显著的治疗作用,可能通过调节抗氧化状态和调节炎症级联反应来实现。

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