title: Remote ischemic postconditioning protects ischemic brain from injury in rats with focal cerebral ischemia/reperfusion associated with suppression of TLR4 and NF-кB expression.
abstract: Remote ischemic postconditioning (RIPC) has been proven to be a promising protective method for brain damage caused by transient focal ischemia/reperfusion (I/R) injury. However, the underlying mechanism of RIPC remains elusive. To address whether RIPC protects against brain damage by regulating TLR4 and the NF-κB pathway, focal I/R rat (SD) model induced by 1 h transient middle cerebral artery occlusion was used in this study. RIPC treatment was generated by three cycles of 10 min occlusion and 10 min release of the bilateral hind femoral arteries. The Garcia JH score was used to evaluate neurobehavioral function and triphenyltetrazolium chloride staining was used to estimate the infarct size of the brain. The expression levels of TLR4 and NF-κB were determined by quantitative PCR and immunohistochemistry. The results showed that RIPC treatment significantly improved neurological deficits and decreased infarct volume. Furthermore, it also inhibited the overexpression of TLR4 and NF-κB induced by middle cerebral artery occlusion reperfusion. Thus, we suggested that RIPC might protect ischemic brain against I/R injury in rats by suppressing the TLR4/NF-кB pathway.
authors.affiliation: aDepartment of Morphology Lab, Chengdu Medical College bState Key Laboratory of Medical Neurobiology, Sichuan University, Chengdu cDepartment of Anatomy Lab, North Sichuan Medical College, Nanchong, Sichuan dInstitute of Neuroscience, Kunming Medical University, Kunming, Yunnan eDepartment of Anatomy, Qinghai University, Xining, Qinghai, China.
authors.forename: Wenqian
authors.initials: W
authors.lastname: Qi
authors.forename: Fangfang
authors.initials: F
authors.lastname: Zhou
authors.forename: Shuai
authors.initials: S
authors.lastname: Li
authors.forename: Yonghua
authors.initials: Y
authors.lastname: Zong
authors.forename: Mingxiao
authors.initials: M
authors.lastname: Zhang
authors.forename: Yousheng
authors.initials: Y
authors.lastname: Lin
authors.forename: Xiao
authors.initials: X
authors.lastname: Zhang
authors.forename: Huijun
authors.initials: H
authors.lastname: Yang
authors.forename: Yu
authors.initials: Y
authors.lastname: Zou
authors.forename: Cunfang
authors.initials: C
authors.lastname: Qi
authors.forename: Tinghua
authors.initials: T
authors.lastname: Wang
authors.forename: Xiaosong
authors.initials: X
authors.lastname: Hu
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000150:complications*; D002545:Brain Ischemia / Q000209:etiology / Q000378:metabolism*; D005260:Female; D057775:Ischemic Postconditioning; D016328:NF-kappa B / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury; D051197:Toll-Like Receptor 4 / Q000378:metabolism*
chemical_list: D016328:NF-kappa B; D012333:RNA, Messenger; C495347:Tlr4 protein, rat; D051197:Toll-Like Receptor 4