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从紫色杆菌中分离出的紫菌素对吲哚美辛诱导的大鼠胃损伤的胃保护活性:潜在作用机制的研究

Gastroprotective activity of violacein isolated from Chromobacterium violaceum on indomethacin-induced gastric lesions in rats: investigation of potential mechanisms of action.

作者信息

Antonisamy Paulrayer, Kannan Ponnusamy, Aravinthan Adithan, Duraipandiyan Veeramuthu, Arasu Mariadhas Valan, Ignacimuthu Savarimuthu, Al-Dhabi Naif Abdullah, Kim Jong-Hoon

机构信息

Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, 664-14 1GA, Duck Jin-Dong, Deokjin-gu, Jeonju City, Jeollabuk-do 561-756, Republic of Korea.

Division of Ethnopharmacology, Entomology Research Institute, Loyola College, Chennai, Tamil Nadu 600 034, India.

出版信息

ScientificWorldJournal. 2014;2014:616432. doi: 10.1155/2014/616432. Epub 2014 Aug 5.

Abstract

Chromobacterium violaceum, Gram-negative bacteria species found in tropical regions of the world, produces a distinct deep violet-colored pigment called violacein. In the present study, we investigated whether violacein can promote a gastroprotective effect and verified the possible mechanisms involved in this action. For this study, an indomethacin-induced gastric ulcer rat model was used. The roles of biomolecules such as MPO, PGE2, pro- and anti-inflammatory cytokines, growth factors, caspase-3, NO, K(+)ATP channels, and α 2-receptors were investigated. Violacein exhibited significant gastroprotective effect against indomethacin-induced lesions, while pretreatment with L-NAME and glibenclamide (but not with NEM or yohimbine) was able to reverse this action. Pretreatment with violacein also restored cNOS level to normal and led to attenuation of enhanced apoptosis and gastric microvascular permeability. Our results suggest that violacein provides a significant gastroprotective effect in an indomethacin-induced ulcer model through the maintenance of some vital protein molecules, and this effect appears to be mediated, at least in part, by endogenous prostaglandins, NOS, K(+)ATP channel opening, and inhibition of apoptosis and gastric microvascular permeability.

摘要

紫色杆菌是一种革兰氏阴性菌,存在于世界热带地区,能产生一种名为紫菌素的独特深紫色色素。在本研究中,我们调查了紫菌素是否能发挥胃保护作用,并验证了这一作用涉及的可能机制。本研究使用了吲哚美辛诱导的胃溃疡大鼠模型。研究了髓过氧化物酶(MPO)、前列腺素E2(PGE2)、促炎和抗炎细胞因子、生长因子、半胱天冬酶-3、一氧化氮(NO)、钾离子ATP通道和α2受体等生物分子的作用。紫菌素对吲哚美辛诱导的损伤表现出显著的胃保护作用,而用L-硝基精氨酸甲酯(L-NAME)和格列本脲预处理(但用N-乙基马来酰亚胺(NEM)或育亨宾预处理则不能)能够逆转这一作用。用紫菌素预处理还能使内皮型一氧化氮合酶(cNOS)水平恢复正常,并减轻增强的细胞凋亡和胃微血管通透性。我们的结果表明,紫菌素通过维持一些重要的蛋白质分子,在吲哚美辛诱导的溃疡模型中发挥显著的胃保护作用,并且这种作用似乎至少部分是由内源性前列腺素、一氧化氮合酶、钾离子ATP通道开放以及对细胞凋亡和胃微血管通透性的抑制介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1835/4138890/49cdf7aa5583/TSWJ2014-616432.001.jpg

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