丙酸钠通过抑制NLRP3保护脓毒症大鼠的结肠组织

doi:10.3969/j.issn.2095-9400.2020.09.005

Abstract
Figure/Table
References (20)
Related Citation (15)

Download: PDF (2353 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective: To explore the protective effect of sodium propionate (SP) on colon tissue of septic rats and study its relationship with NLRP3 inflammasomes. Methods: Animal models of sepsis were established by cecum ligation and puncture (CLP) and randomly divided as sham operation group, model group, model+SP group and sham operation+SP group. Rats of each group were sacrificed 24 hours after modeling, and colonic tissues were collected. HE staining was used to observe the changes of colonic structure in each group of rats and ELISA kit to detect IL-6, TGF-β and TNF-α levels in colon tissue. Western blot and immunohistochemical staining were used to detect the expression of claudin-1 and occludin and NLRP3 inflammasomes. The same method was used to establish a sepsis model, and the 72 h survival rate of each group of rats was recorded. Results: SP treatment could improve the survival rate and reduce pathological damage in the model group. The levels of IL-6, TGF-β and TNF-α in colon tissue of model+SP group were lower than those of the model group. Compared with the model group, the expression of claudin-1 and occludin in the colon tissue of the model+SP group increased. The expressions of NLRP3, caspase-1, IL-β and IL-18 in colon tissue of model+SP group were significantly lower than those of the model group. Conclusion: SP can improve the survival rate of sepsis rats. In addition, SP reduces colon injury by increasing the expression of tight junction proteins in the colon tissue of sepsis rats and inhibiting the activation of NLRP3 inflammatory inflammasomes.

Key words： sodium propionate tight junction proteins NLRP3 inflammasomes sepsis rats

Received: 22 April 2020

	Service
	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	XIE Xianzheng
	YANG Randong
	CHEN Xiaoming

URL:

https://xb.wmu.edu.cn/EN/10.3969/j.issn.2095-9400.2020.09.005 OR https://xb.wmu.edu.cn/EN/Y2020/V50/I9/712

[1] FALAGAS M E, KORBILA I P, KAPASKELIS A, et al. Trends of mortality due to septicemia in Greece: an 8-year analysis[J]. PLoS One, 2013, 8(7): e67621.
[2] ROSSAINT J, ZARBOCK A. Pathogenesis of multiple organ failure in sepsis[J]. Crit Rev Immunol, 2015, 35(4): 277-291.
[3] HASSOUN H T, KONE B C, MERCER D W, et al. Post-injury multiple organ failure: the role of the gut[J]. Shock, 2001, 15(1): 1-10.
[4] CANI P D, NEYRINCK A M, FAVA F, et al. Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia[J]. Diabetologia, 2007, 50(11): 2374-2383.
[5] 陈泳祥, 梁俊文, 严建威. 脓毒症患者外周血单核细胞NLRP3炎性小体的表达研究[J]. 临床急诊杂志, 2019, 20(4): 292-297.
[6] 林日添, 吴维, 刘占举. 短链脂肪酸对肠黏膜稳态免疫调节作用的研究进展[J]. 免疫学杂志, 2017(10): 900-904.
[7] TAN J, MCKENZIE C, POTAMITIS M, et al. The role of short-chain fatty acids in health and disease[J]. Adv Immunol, 2014, 121: 91-119.
[8] TONG L C, WANG Y, WANG Z B, et al. Propionate ameliorates dextran sodium sulfate-induced colitis by improving intestinal barrier function and reducing inflammation and oxidative stress[J]. Front Pharmacol, 2016, 7: 253.
[9] TEDELIND S, WESTBERG F, KJERRULF M, et al. Anti-inflammatory properties of the short-chain fatty acids acetate and propionate: a study with relevance to inflammatory bowel disease[J]. World J Gastroenterol, 2007, 13(20): 2826-2832.
[10] XIA Z, HAN Y, WANG K, et al. Oral administration of propionic acid during lactation enhances the colonic barrier function[J]. Lipids Health Dis, 2017, 16(1): 62.
[11] MENG M, KLINGENSMITH N J, COOPERSMITH C M. New insights into the gut as the driver of critical illness and organ failure[J]. Curr Opin Crit Care, 2017, 23(2): 143-148.
[12] CHOUSTERMAN B G, SWIRSKI F K, WEBER G F. Cytokine storm and sepsis disease pathogenesis[J]. Semin Immunopathol, 2017, 39(5): 517-528.
[13] MISHRA S K, CHOUDHURY S. Experimental protocol for cecal ligation and puncture model of polymicrobial sepsis and assessment of vascular functions in mice[J]. Methods Mol Biol, 2018, 1717: 161-187.
[14] AKSOY A N, TOKER A, CELIK M, et al. The effect of progesterone on systemic inflammation and oxidative stress in the rat model of sepsis[J]. Indian J Pharmacol, 2014, 46(6): 622-626.
[15] KUMARI A, DASH D, SINGH R. Curcumin inhibits lipopolysaccharide (LPS)-induced endotoxemia and airway inflammation through modulation of sequential release of inflammatory mediators (TNF-α and TGF-β1) in murine model[J]. Inflammopharmacology, 2017, 25(3): 329-341.
[16] FURUSE M, HATA M, FURUSE K, et al. Claudin-based tight junctions are crucial for the mammalian epidermal barrier: a lesson from claudin-1-deficient mice[J]. J Cell Biol, 2002, 156(6): 1099-1111.
[17] KAUKONEN K-M, BAILEY M, BELLOMO R. Systemic inflammatory response syndrome criteria for severe sepsis [J]. N Engl J Med, 2015, 373(9): 881.
[18] 曹莉. 脓毒症炎症级联反应及分子学干预研究进展[J]. 内科, 2019, 14(3): 317-320.
[19] ESQUERDO K F, SHARMA N K, BRUNIALTI M K C, et al. Inflammasome gene profile is modulated in septic patients, with a greater magnitude in non-survivors[J]. Clin Exp Immunol, 2017, 189(2): 232-240.
[20] MACIA L, TAN J, VIEIRA A T, et al. Metabolite-sensing receptors GPR43 and GPR109A facilitate dietary fibre-induced gut homeostasis through regulation of the inflammasome[J]. Nat Commun, 2015, 6: 6734.