科研成果详情

题名Micheliolide ameliorates severe acute pancreatitis in mice through potentiating Nrf2-mediated anti-inflammation and anti-oxidation effects
作者
发表日期2024-12-25
发表期刊INTERNATIONAL IMMUNOPHARMACOLOGY   影响因子和分区
语种英语
原始文献类型Article
关键词Micheliolide Severe acute pancreatitis Nuclear factor erythroid 2-related factor 2 Nuclear factor kappa B p65
其他关键词NF-KAPPA-B ; OXIDATIVE STRESS ; PATHOGENESIS ; AUTOPHAGY
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.
资助项目Wenzhou Science and Technology bureau [Y2020231]; Natural Science Foundation of Zhe-jiang province [LQ23H050001, ZCLQ24H0303]; National Nat-ural Sciences Foundation of China [82070834]
出版者ELSEVIER
ISSN1567-5769
EISSN1878-1705
卷号143期号:Pt 2
DOI10.1016/j.intimp.2024.113490
页数13
WOS类目Immunology ; Pharmacology & Pharmacy
WOS研究方向Immunology ; Pharmacology & Pharmacy
WOS记录号WOS:001347351000001
收录类别SCIE ; SCOPUS ; PUBMED
URL查看原文
PubMed ID39467351
SCOPUSEID2-s2.0-85207170320
通讯作者地址[Lu, Chao-Sheng;Hu, Qing-Qing]Wenzhou Med Univ, Affiliated Hosp 1, Dept Pediat, 322 Nanbaixiang St, Wenzhou 325000, Zhejiang, Peoples R China.
Scopus学科分类Immunology and Allergy;Immunology;Pharmacology
SCOPUS_IDSCOPUS_ID:85207170320
引用统计
文献类型期刊论文
条目标识符https://kms.wmu.edu.cn/handle/3ETUA0LF/221443
专题附属第一医院_儿科
第一临床医学院(信息与工程学院)、附属第一医院
附属第一医院
第一临床医学院(信息与工程学院)、附属第一医院_外科学_甲状腺外科
通讯作者Lu, Chao-Sheng; Hu, Qing-Qing
作者单位
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
第一作者单位附属第一医院_儿科;  附属第一医院
通讯作者单位附属第一医院_儿科
第一作者的第一单位附属第一医院_儿科
推荐引用方式
GB/T 7714
Wu, Chen-Yu,Wang, Ke-Qi,Qin, Yu-Ying,et al. Micheliolide ameliorates severe acute pancreatitis in mice through potentiating Nrf2-mediated anti-inflammation and anti-oxidation effects[J]. INTERNATIONAL IMMUNOPHARMACOLOGY,2024,143(Pt 2).
APA Wu, Chen-Yu., Wang, Ke-Qi., Qin, Yu-Ying., Wang, Hong-Wei., Wu, Min-Min., ... & Hu, Qing-Qing. (2024). Micheliolide ameliorates severe acute pancreatitis in mice through potentiating Nrf2-mediated anti-inflammation and anti-oxidation effects. INTERNATIONAL IMMUNOPHARMACOLOGY, 143(Pt 2).
MLA Wu, Chen-Yu,et al."Micheliolide ameliorates severe acute pancreatitis in mice through potentiating Nrf2-mediated anti-inflammation and anti-oxidation effects".INTERNATIONAL IMMUNOPHARMACOLOGY 143.Pt 2(2024).

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