Micheliolide ameliorates severe acute pancreatitis in mice through potentiating Nrf2-mediated anti-inflammation and anti-oxidation effects

被引:2
|
作者
Wu, Chen-Yu [1 ,2 ]
Wang, Ke-Qi [1 ,2 ]
Qin, Yu-Ying [1 ,2 ]
Wang, Hong-Wei [2 ]
Wu, Min-Min [2 ]
Zhu, Xian-Dong [3 ]
Lu, Xin-Yu [2 ,4 ]
Zhu, Mian-Mian [1 ,2 ]
Lu, Chao-Sheng [1 ,2 ]
Hu, Qing-Qing [1 ,2 ]
机构
[1] Wenzhou Med Univ, Affiliated Hosp 1, Dept Pediat, 322 Nanbaixiang St, Wenzhou 325000, Zhejiang, Peoples R China
[2] Wenzhou Med Univ, Affiliated Hosp 1, Zhejiang Key Lab Intelligent Canc Biomarker Discov, Wenzhou 325000, Peoples R China
[3] Wenzhou Med Univ, Affiliated Hosp 1, Dept Thyroid Surg, Wenzhou 325000, Peoples R China
[4] Wenzhou Med Univ, Clin Med Coll 1, Wenzhou 325000, Peoples R China
关键词
Micheliolide; Severe acute pancreatitis; Nuclear factor erythroid 2-related factor 2; Nuclear factor kappa B p65; NF-KAPPA-B; OXIDATIVE STRESS; PATHOGENESIS; AUTOPHAGY;
D O I
10.1016/j.intimp.2024.113490
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Severe acute pancreatitis (SAP) is an acute inflammatory injury disease with significant mortality rate and currently without effective strategy being available. Inflammation and oxidative stress play central roles in the etiology of SAP. Micheliolide (MCL), an active monomeric component isolated from Michelia champaca, has been proved its multiple therapeutic properties including anti-inflammatory, antioxidant and anti-cancer. Nevertheless, the therapeutic effect and underlying mechanism of MCL in SAP still remain unclear. Here, we found that caerulein with lipopolysaccharide (LPS)-induced SAP murine models exhibited severe pancreatic injury, including necrosis, edema, and vacuolation of acinar cells in the pancreas, elevated serum levels of amylase and lipase, and reduced number of the exocrine cells. As expected, MCL treatment alleviated these side effects. Mechanistically, MCL triggered nuclear factor erythroid 2-related factor 2 (Nrf2) activation, thereby activating Nrf2-regulated antioxidative pathways and inhibiting nuclear factor kappa B p65 (NF-kappa B p65)-mediated inflammatory response, resulting in protection against pancreatic injury in SAP mice. In addition, Nrf2 gene deficiency abolished the beneficial effects of MCL on SAP-induced pancreatic inflammation and oxidative stress and blocked the ability of MCL to alleviate the pancreatic injury in SAP mice. Collectively, these findings indicated that the suppression of SAP-induced pancreatic injury by MCL was at least in part due to Nrf2-mediated anti-oxidation effect and inhibition of inflammation.
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页数:13
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