Corilagin alleviates intestinal ischemia/reperfusion-induced intestinal and lung injury in mice via inhibiting NLRP3 inflammasome activation and pyroptosis

Abstract

Intestinal ischemia reperfusion (II/R) is a clinical emergency that frequently occurs in a variety of clinical conditions. Severe intestinal injury results in the release of cytotoxic substances and inflammatory mediators which can activate local inflammatory response and bacterial translocation. This triggers multi-organ failure, including lung injury, which is a common complication of II/R injury and contributes to the high mortality rate. Corilagin (Cor) is a natural ellagitannin found in a variety of plants. It has many biological and pharmacological properties, including antioxidant, anti-inflammatory and anti-apoptosis activities. However, no studies have evaluated the effects and molecular mechanisms of Cor in alleviating II/R-induced intestinal and lung damage. In this study, Cor was found to significantly alleviate II/R-induced pathological damage, inflammatory response, oxidative stress, NLRP3 inflammasome activation, and pyroptosis in intestinal and lung tissues both in vivo and in vitro. Further, Cor inhibited the NLRP3 inflammasome activation and pyroptosis in RAW264.7 and MLE-12 cells induced by LPS/nigericin and that in IEC-6 cells induced by nigericin, indicating an amelioration of Cor in II/R-induced intestinal and lung injury via inhibiting NLRP3 inflammasome activation and pyroptosis. Thus, Cor might be a potential therapeutic agent for II/R-induced inflammation and tissue injury.

NET-Related Gene as Potential Diagnostic Biomarkers for Diabetic Tubulointerstitial Injury

“…Activated macrophages can also secrete TNF-α and CCL2 to recruit more neutrophils [8], perpetuating a positive feedback loop exacerbating disease. Moreover, macrophage engulfment of mast cell granules may suppress excess activation [38], consistent with our findings that targeting CASP1/LYZ could ameliorate aberrant immunity and arrest DKD tubulointerstitial injury.…”

Corilagin alleviates atherosclerosis by inhibiting NLRP3 inflammasome activation via the Olfr2 signaling pathway in vitro and in vivo

“…In conjunction with TLR4, Olfr2 expressed in mouse vascular macrophages can active NLRP3 inflammasome to promote the development of atherosclerosis (35). According to previous findings, Corilagin can inhibit NLRP3 inflammasome activation and pyroptosis in ischemia-reperfusion induced intestinal and lung injury (38), and ameliorate atherosclerosis by restraining the TLR4 signaling pathway (17,40). Consequently, this study aims to explore whether Corilagin can influence atherosclerosis through the Olfr2 signaling pathway.…”

“…Corilagin, a polyphenolic monomer isolated from Phyllanthus urinaria, exhibits diverse pharmacological properties including antitumor, antioxidant, and anti-inflammatory effects ( 17 , 36 ). It can ameliorate inflammatory lesions in macrophages by inhibiting NLRP3 inflammasome activation and pyroptosis ( 37 , 38 ). Nonetheless, the specific impact of Corilagin on NLRP3 inflammasome activation in atherosclerosis necessitates further investigation.…”

Advancements in the study of acute lung injury resulting from intestinal ischemia/reperfusion

“…Currently, prominent traditional Chinese medicine treatments for II/R-induced systemic diseases include conventional Chinese medicine treatment and acupuncture treatment. The effectiveness of Artesunate (18), Corilagin (17,118), and Nervilifordin F (30), active ingredients of Artemisia annua, ellagic tannin, and Nervilia fordii, has been confirmed in preclinical studies of II/R-related diseases. The potential mechanism aligns with the aspects mentioned above.…”