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CLC number: R574

On-line Access: 2016-03-07

Received: 2015-10-11

Revision Accepted: 2015-12-09

Crosschecked: 2016-02-15

Cited: 1

Clicked: 1880

Citations:  Bibtex RefMan EndNote GB/T7714

 ORCID:

Xi-shuang Liu

http://orcid.org/0000-0002-5177-3535

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Journal of Zhejiang University SCIENCE B 2016 Vol.17 No.3 P.209-217

http://doi.org/10.1631/jzus.B1500248


Hydrogen sulfide from a NaHS source attenuates dextran sulfate sodium (DSS)-induced inflammation via inhibiting nuclear factor-κB


Author(s):  Xi Chen, Xi-shuang Liu

Affiliation(s):  Medical College, Qingdao University, Qingdao 266021, China; more

Corresponding email(s):   liunich2015@126.com

Key Words:  Hydrogen sulfide (H2S), Inflammation, Nuclear factor-κ, B (NF-κ, B), Dextran sulfate sodium (DSS)


Xi Chen, Xi-shuang Liu. Hydrogen sulfide from a NaHS source attenuates dextran sulfate sodium (DSS)-induced inflammation via inhibiting nuclear factor-κB[J]. Journal of Zhejiang University Science B, 2016, 17(3): 209-217.

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T1 - Hydrogen sulfide from a NaHS source attenuates dextran sulfate sodium (DSS)-induced inflammation via inhibiting nuclear factor-κB
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DOI - 10.1631/jzus.B1500248


Abstract: 
This study investigated the alleviating effects of hydrogen sulfide (H2S), derived from sodium hydrosulfide (NaHS), on inflammation induced by dextran sulfate sodium (DSS) in both in vivo and in vitro models. We found that NaHS injection markedly decreased rectal bleeding, diarrhea, and histological injury in DSS-challenged mice. NaHS (20 μmol/L) reversed DSS-induced inhibition in cell viability in Caco-2 cells and alleviated pro-inflammation cytokine expression in vivo and in vitro, indicating an anti-inflammatory function for H2S. It was also found that H2S may regulate cytokine expression by inhibiting the nuclear factor-κ;b (NF-κ;b) signaling pathway. In conclusion, our results demonstrated that H2S alleviated DSS-induced inflammation in vivo and in vitro and that the signal mechanism might be associated with the NF-κB signaling pathway.

硫化氢通过抑制NF-κB信号通路对葡聚糖硫酸钠(DSS)诱导的炎症反应起到缓解效果

目的:硫化氢(H2S)具有抗氧化和抗炎反应的作用,但是在DSS诱导的结肠炎模型中的研究鲜有报道。因此,本文采用小鼠和人结肠上皮细胞系Caco-2为实验模型,研究了H2S在DSS诱导的炎症模型中的缓解效果。
创新点:(1)本研究采用体内和体外模型分别对H2S对DSS诱导的炎症缓解效果进行了验证,结果发现H2S具有抗炎作用;(2)本研究发现H2S能够抑制核转录因子κB(NF-κB)信号通路,从而对炎症起到缓解作用。
方法:采用DSS建立小鼠结肠炎模型,腹腔注射H2S供体硫化氢钠(NaHS);采用DSS诱导Caco-2炎症,然后处理H2S供体NaHS。收集小鼠结肠组织和细胞,进行反转录聚合酶链反应(RT-PCR)和蛋白质免疫印迹法(Western blot)分析炎症基因和NF-κB表达情况。
结论:H2S对DSS诱导的体内和体外炎症反应具有一定的缓解作用,其机制可能是通过影响了NF-κB信号通路。

关键词:硫化氢(H2S);炎症反应;核转录因子κB(NF-κB);葡聚糖硫酸钠(DSS)

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference

[1]Beloqui, A., Coco, R., Alhouayek, M., et al., 2013. Budesonide-loaded nanostructured lipid carriers reduce inflammation in murine DSS-induced colitis. Int. J. Pharm., 454(2):775-783.

[2]Benetti, L.R., Campos, D., Gurgueira, S.A., et al., 2013. Hydrogen sulfide inhibits oxidative stress in lungs from allergic mice in vivo. Eur. J. Pharmacol., 698(1-3):463-469.

[3]Bhatia, M., 2015. H2S and inflammation: an overview. In: Moore, P.K., Whiteman, M. (Eds.), Chemistry, Biochemistry and Pharmacology of Hydrogen Sulfide. Springer International Publishing, Switzerland, p.165-180.

[4]Cao, A.T., Yao, S., Stefka, A.T., et al., 2014. TLR4 regulates IFN-γ and IL-17 production by both thymic and induced Foxp3+ Tregs during intestinal inflammation. J. Leukoc. Biol., 96(5):895-905.

[5]Cheon, J.H., Kim, J.S., Kim, J.M., et al., 2006. Plant sterol guggulsterone inhibits nuclear factor-κB signaling in intestinal epithelial cells by blocking IκB kinase and ameliorates acute murine colitis. Inflamm. Bowel Dis., 12(12):1152-1161.

[6]Dubeau, M.F., Iacucci, M., Beck, P.L., et al., 2013. Drug-induced inflammatory bowel disease and IBD-like conditions. Inflamm. Bowel Dis., 19(2):445-456.

[7]Eastep, J., Chen, G., 2015. The relationships of high-fat diet and metabolism of lipophilic vitamins. Integr. Food Nutr. Metab., 2(3):174-179.

[8]Flannigan, K.L., Agbor, T.A., Blackler, R.W., et al., 2014. Impaired hydrogen sulfide synthesis and IL-10 signaling underlie hyperhomocysteinemia-associated exacerbation of colitis. PNAS, 111(37):13559-13564.

[9]Furne, J.K., Suarez, F.L., Ewing, S.L., et al., 2000. Binding of hydrogen sulfide by bismuth does not prevent dextran sulfate-induced colitis in rats. Digest. Dis. Sci., 45(7):1439-1443.

[10]Gemici, B., Elsheikh, W., Feitosa, K.B., et al., 2015. H2S-releasing drugs: anti-inflammatory, cytoprotective and chemopreventative potential. Nitric Oxide, 46:25-31.

[11]Hirai, F., Matsui, T., 2015. Status of food intake and elemental nutrition in patients with Crohn’s disease. Integr. Food Nutr. Metab., 2(2):148-150.

[12]Hirata, I., Naito, Y., Takagi, T., et al., 2011. Endogenous hydrogen sulfide is an anti-inflammatory molecule in dextran sodium sulfate-induced colitis in mice. Digest. Dis. Sci., 56(5):1379-1386.

[13]Howell, K., Yan, F., Tokich, A., et al., 2015. Iron sequestration is not the main mechanism in the inhibition of Staphylococcus aureus growth by cranberry phytochemicals. Integr. Food Nutr. Metab., 2(3):184-188.

[14]Kabil, O., Motl, N., Banerjee, R., 2014. H2S and its role in redox signaling. Biochim. Biophys. Acta, 1844(8):1355-1366.

[15]Kaplan, G.G., 2015. The global burden of IBD: from 2015 to 2025. Nat. Rev. Gastroenterol. Hepatol., 12:720-727.

[16]Kimura, Y., Kimura, H., 2004. Hydrogen sulfide protects neurons from oxidative stress. FASEB J., 18(10):1165-1167.

[17]Lee, S.W., Hu, Y.S., Hu, L.F., et al., 2006. Hydrogen sulphide regulates calcium homeostasis in microglial cells. Glia, 54(2):116-124.

[18]Liu, L., Xiao, Q.F., Zhang, Y.L., et al., 2014. A cross-sectional study of irritable bowel syndrome in nurses in China: prevalence and associated psychological and lifestyle factors. J. Zhejiang Univ.-Sci. B (Biomed. & Biotechnol.), 15(6):590-597.

[19]Malago, J.J., Sangu, C.L., 2015. Intraperitoneal administration of butyrate prevents the severity of acetic acid colitis in rats. J. Zhejiang Univ.-Sci. B (Biomed. & Biotechnol.), 16(3):224-234.

[20]McCann, M.J., Dalziel, J.E., Bibiloni, R., et al., 2015. An integrated approach to assessing the bio-activity of nutrients in vitro: the anti-oxidant effects of catechin and chlorogenic acid as an example. Integr. Food Nutr. Metab., 2(3):197-204.

[21]Mikami, Y., Shibuya, N., Kimura, Y., et al., 2011. Hydrogen sulfide protects the retina from light-induced degeneration by the modulation of Ca2+ influx. J. Biol. Chem., 286(45):39379-39386.

[22]Mileva, S., Galunska, B., Gospodinova, M., et al., 2014. Vitamin D3 status in children with acute diarrhea. Integr. Food Nutr. Metab., 1(2):1-6.

[23]Nighot, P., Young, K., Nighot, M., et al., 2013. Chloride channel ClC-2 is a key factor in the development of DSS-induced murine colitis. Inflamm. Bowel Dis., 19(13):2867-2877.

[24]Novokmet, M., Lukic, E., Vuckovic, F., et al., 2014. Changes in IgG and total plasma protein glycomes in acute systemic inflammation. Sci. Rep., 4:4347.

[25]Pozsgai, G., Benko, R., Bartho, L., et al., 2015. Thermal spring water drinking attenuates dextran-sulfate-sodium-induced colitis in mice. Inflammopharmacology, 23(1):57-64.

[26]Rashti, Z., Koohsari, H., 2015. Antibacterial effects of supernatant of lactic acid bacteria isolated from different Dough’s in Gorgan city in north of Iran. Integr. Food Nutr. Metab., 2(3):193-196.

[27]Sánchez-Fidalgo, S., Cardeno, A., Sanchez-Hidalgo, M., et al., 2013. Dietary extra virgin olive oil polyphenols supplementation modulates DSS-induced chronic colitis in mice. J. Nutr. Biochem., 24(7):1401-1413.

[28]Scharl, M., Vavricka, S.R., Rogler, G., 2013. Review: new anti-cytokines for IBD: what is in the pipeline Curr. Drug Targets, 14(12):1405-1420.

[29]Shimshoni, E., Yablecovitch, D., Baram, L., et al., 2015. ECM remodelling in IBD: innocent bystander or partner in crime The emerging role of extracellular molecular events in sustaining intestinal inflammation. Gut, 64(3):367-372.

[30]Shin, H.S., Kang, S.I., Yoon, S.A., et al., 2012. Sinensetin attenuates LPS-induced inflammation by regulating the protein level of IκB-α. Biosci. Biotechnol. Biochem., 76(4):847-849.

[31]Shori, A.B., Baba, A.S., 2015. Fermented milk derives bioactive peptides with antihypertensive effects. Integr. Food Nutr. Metab., 2(3):178-181.

[32]Sun, X.F., Zhang, H., 2007. NFKB and NFKBI polymorphisms in relation to susceptibility of tumour and other diseases. Histol. Histopathol., 22(12):1387-1398.

[33]Sunil, Y., Ramadori, G., Raddatzc, D., 2010. Influence of NFκB inhibitors on IL-1β-induced chemokine CXCL8 and -10 expression levels in intestinal epithelial cell lines: glucocorticoid ineffectiveness and paradoxical effect of PDTC. Int. J. Colorectal Dis., 25(3):323-333.

[34]Vinod, V.P., Guruvayoorappan, C., 2014. Protective effect of marine mangrove Rhizophora apiculata on acetic acid induced experimental colitis by regulating anti-oxidant enzymes, inflammatory mediators and nuclear factor-κB subunits. Int. Immunopharmacol., 18(1):124-134.

[35]Vlantis, K., Polykratis, A., Welz, P.S., et al., 2015. TLR-independent anti-inflammatory function of intestinal epithelial TRAF6 signalling prevents DSS-induced colitis in mice. Gut, online.

[36]Wang, W., Xia, T., Yu, X., 2015. Wogonin suppresses inflammatory response and maintains intestinal barrier function via TLR4-MyD88-TAK1-mediated NF-κB pathway in vitro. Inflamm. Res., 64(6):423-431.

[37]Watanabe, T., Sato, T., Miyazaki, M., et al., 2015. Effect of body composition intake with nano-lactic acid in rats. Integr. Food Nutr. Metab., 2(2):156-158.

[38]Wu, J., Wei, J., You, X., et al., 2013. Inhibition of hydrogen sulfide generation contributes to lung injury after experimental orthotopic lung transplantation. J. Surg. Res., 182(1):e25-e33.

[39]Xu, W., Chen, J., Lin, J., et al., 2015. Exogenous H2S protects H9c2 cardiac cells against high glucose-induced injury and inflammation by inhibiting the activation of the NF-κB and IL-1β pathways. Int. J. Mol. Med., 35(1):177-186.

[40]Yan, F., Polk, D.B., 1999. Aminosalicylic acid inhibits IκB kinase α phosphorylation of IκBα in mouse intestinal epithelial cells. J. Biol. Chem., 274(51):36631-36636.

[41]Yin, J., Ren, W., Liu, G., et al., 2013a. Birth oxidative stress and the development of an antioxidant system in newborn piglets. Free Radic. Res., 47(12):1027-1035.

[42]Yin, J., Ren, W.K., Wu, X.S., et al., 2013b. Oxidative stress-mediated signaling pathways: a review. J. Food Agric. Environ., 11(2):132-139.

[43]Yin, J., Wu, M.M., Xiao, H., et al., 2014. Development of an antioxidant system after early weaning in piglets. J. Anim. Sci., 92(2):612-619.

[44]Yin, J., Liu, M., Ren, W., et al., 2015a. Effects of dietary supplementation with glutamate and aspartate on diquat-induced oxidative stress in piglets. PLoS ONE, 10(4):e0122893.

[45]Yin, J., Duan, J., Cui, Z., et al., 2015b. Hydrogen peroxide-induced oxidative stress activates NF-κB and Nrf2/Keap1 signals and triggers autophagy in piglets. RSC Adv., 5(20):15479-15486.

[46]Xu, X.J., Liu, L., Yao, S.K., 2016. Nerve growth factor and diarrhea-predominant irritable bowel syndrome (IBS-D): a potential therapeutic target J. Zhejiang Univ.-Sci. B (Biomed. & Biotechnol.), 17(1):1-9.

[47]Zayachkivska, O., Havryluk, O., Hrycevych, N., et al., 2014. Cytoprotective effects of hydrogen sulfide in novel rat models of non-erosive esophagitis. PLoS ONE, 9(10):e110688.

[48]Zhang, P., Li, F., Wiegman, C.H., et al., 2015. Inhibitory effect of hydrogen sulfide on ozone-induced airway inflammation, oxidative stress, and bronchial hyperresponsiveness. Am. J. Resp. Cell Mol. Biol., 52(1):129-137.

[49]Zhou, X., Feng, Y., Zhan, Z., et al., 2014. Hydrogen sulfide alleviates diabetic nephropathy in a streptozotocin-induced diabetic rat model. J. Biol. Chem., 289(42):8827-8834.

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