AI Article Synopsis
- Acute pancreatitis (AP) is a serious condition involving inflammation of the pancreas, and the effects of the compound Lonicerin (LCR) in this context are largely unexplored.
- * In laboratory studies, LCR was found to reduce cell damage and improve cell survival in pancreatic cell models exposed to caerulein (CAE), suggesting it has protective properties against AP.
- * The protective effects of LCR are linked to its ability to influence specific signaling pathways, particularly by lowering harmful inflammation and cell death mechanisms through the activation of SIRT1 and GPX4 proteins.
Article Abstract
Acute pancreatitis (AP) is a familiar emergency of digestive system characterized by pancreatic inflammation. Lonicerin (LCR) has been reported to exert anti-inflammatory and immunomodulatory characteristics in several inflammatory diseases. Nevertheless, its role and mechanism involved in AP are still unknown. This study was designed to explore the protective effect and potential mechanism of LCR in AP. In this study, LCR and ferrostatin-1 alleviated, but erastin aggravated caerulein (CAE) exposure-induced cytotoxicity and reduction of cell viability in AR42J cells. LCR exhibited a protective role in CAE-treated AR42J cells, as evidenced by alleviation of apoptosis, inflammation, and ferroptosis. Mechanistically, LCR decreased the phosphorylation level of nuclear factor-kappa B p65 and increased the levels of silent information regulator 1 (SIRT1) and glutathione peroxidase 4 (GPX4) in CAE-treated AR42J cells. Furthermore, functional rescue experiments manifested that knockdown of SIRT1 partially negated the inhibitory action of LCR against CAE-induced apoptosis, inflammation, and ferroptosis in AR42J cells. Overall, LCR mitigates apoptosis, inflammation, and ferroptosis in CAE-exposed AR42J cells, which is related to the activation of the SIRT1/GPX4 signaling pathway.
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| http://dx.doi.org/10.1016/j.taap.2024.117136 | DOI Listing |
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