Neuroprotection of beta-caryophyllene against cerebral ischemia/reperfusion injury by inhibiting P38 MAPK/NLRP3 signaling pathway

作者全名："Zhao, Hongxia; Deng, Ling; Chen, Sha; Wang, Xuan; Dong, Zhi"

作者地址："[Zhao, Hongxia] Chongqing Gen Hosp, Dept Pharm, Chongqing, Peoples R China; [Zhao, Hongxia; Deng, Ling; Chen, Sha; Wang, Xuan; Dong, Zhi] Chongqing Med Univ, Chongqing Key Lab Biochem & Mol Pharmacol, 1 Yixueyuan Rd, Chongqing 400016, Peoples R China"

通信作者："Dong, Z (通讯作者)，Chongqing Med Univ, Chongqing Key Lab Biochem & Mol Pharmacol, 1 Yixueyuan Rd, Chongqing 400016, Peoples R China."

来源：NEUROREPORT

ESI学科分类：NEUROSCIENCE & BEHAVIOR

WOS号：WOS:001033573000003

JCR分区：Q4

影响因子：1.6

年份：2023

卷号：34

期号：12

开始页：617

结束页：623

文献类型：Article

关键词：cerebral ischemia/reperfusion injury; inflammation; NLRP3 inflammasome; p38 MAPK; beta-caryophyllene

摘要："The main objective of our research was to explore the neuroprotective effect and underlying mechanism of ss-caryophyllene (BCP) pretreatment against cerebral ischemia/reperfusion injury (CIRI). Neurological deficit score, infarct size, and sensorimotor function were assessed 24 h following reperfusion. Additionally, histopathological damage of neurons was evaluated using hematoxylin-eosin staining. The mRNA level of nod-like receptor family pyrin domain-containing 3 (NLRP3) was determined using quantitative real time PCR. The expressions of p-p38, p38, NLRP3, procaspase-1, and ASC (apoptosis-associated speck like protein containing a CARD) were measured using western blot analysis. The levels of interleukin-1 ss (IL-1 ss) and interleukin-18 ( IL-18) were quantified utilizing the ELISA. Our findings indicated that BCP pretreatment significantly reduced the infarct volume, neurologic deficit score, sensorimotor deficits, histopathological damage, and expression of inflammatory factors. Besides, BCP pretreatment effectively suppressed the expression of p-p38, as well as the activation of NLRP3 inflammasome. The administration of anisomycin, an activator of p38 MAPK, was found to notably impede the favorable outcomes conferred by BCP pretreatment, which included reducing the infarct volume, improving the neurologic deficit score, mitigating the sensorimotor deficits, and attenuating the histopathological damage. Furthermore, anisomycin effectively reversed the suppressive impact of BCP on NLRP3 inflammasome activation. This research uncovered that pretreatment with BCP has the potential to alleviate CIRI by effectively suppressing the activation of NLRP3 inflammasome through the p38 MAPK signaling pathway. NeuroReport 34: 617-623 Copyright (c) 2023 Wolters Kluwer Health, Inc. All rights reserved."

基金机构："Natural Science Foundation of Chongqing, China [cstc2018jcyjAX0378]"

基金资助正文："This study was supported by the Natural Science Foundation of Chongqing, China (cstc2018jcyjAX0378)"