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Coptisine attenuates post-infectious IBS via Nrf2-dependent inhibition of the NLPR3 inflammasome.
- Source :
-
Molecular Medicine Reports . Dec2022, Vol. 26 Issue 6, pN.PAG-N.PAG. 1p. - Publication Year :
- 2022
-
Abstract
- Inhibition of the activation of the NLR family pyrin domain-containing 3 (NLRP3) inflammasome has previously been reported to confer protection against post-infectious irritable bowel syndrome (PI–IBS). Coptisine, the second most abundant isoquinoline alkaloid in Coptis chinensis, can inhibit NLRP3 inflammasome activation; however, whether coptisine exhibits protective effects against PI–IBS remains unclear. In the present study, coptisine significantly reduced gastrointestinal motility and abdominal withdrawal reflex scores in a PI–IBS rat model that was induced using intragastric administration of Trichinella spiralis larvae. Coptisine treatment significantly decreased the protein levels of oxidative stress markers, 4-hydroxynonenal, protein carbonyl and 8-hydroxy-2′deoxyguanosine, and proinflammatory cytokines, TNF-α, IL-1β and IL-18 in the colon of PI–IBS rats. Moreover, coptisine treatment significantly increased nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation and heme oxygenase-1 protein expression levels, while significantly downregulating the protein expression levels of NLRP3, apoptosis-associated speck-like protein containing a CARD and caspase-1 in the colons of PI–IBS rats. It is important to note that the anti-inflammatory effects of coptisine were blocked by the Nrf2 inhibitor ML385. In summary, the present study indicated that coptisine potentially attenuated PI–IBS in rats via Nrf2-dependent inhibition of the NLPR3 inflammasome. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 17912997
- Volume :
- 26
- Issue :
- 6
- Database :
- Academic Search Index
- Journal :
- Molecular Medicine Reports
- Publication Type :
- Academic Journal
- Accession number :
- 160234956
- Full Text :
- https://doi.org/10.3892/mmr.2022.12879