Oleanic acid alleviates cerebral ischemia-reperfusion injury in rats by inhibiting the JAK2/STAT3 signaling pathway
10.3760/cma.j.issn.1673-4165.2024.06.005
- VernacularTitle:齐墩果酸通过抑制JAK2/STAT3信号通路减轻大鼠脑缺血再灌注损伤
- Author:
Liqiang YANG
1
;
Weijie XU
;
Xiuying GUAN
;
Xin GUAN
Author Information
1. 昆明卫生职业学院，昆明 650600
- Keywords:
Brain ischemia;
Reperfusion injury;
Oleanic acid;
Neuroprotective agents;
Janus kinase 2;
STAT3 transcription factor;
Signal transduction;
Rats
- From:
International Journal of Cerebrovascular Diseases
2024;32(6):428-434
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the protective effects of oleanic acid (OA) on cerebral ischemia-reperfusion (I/R) injury in rats and the role of JAK2/STAT3 signaling pathway.Methods:Seventy-two adult male SD rats were randomly divided into sham-operation group, model group (I/R), OA group (I/R+OA), and inhibitor group (I/R+OA+FLLL32). The left middle cerebral artery I/R model was constructed by the thread occlusion method. After modeling, OA and JAK2/STAT3 inhibitor FLLL32 were administered via intraperitoneal injection and lateral ventricular injection, respectively, for a total of 7 days. Neurological deficits were evaluated by behavioral methods, infarct volume was detected by 2,3, 5-triphenyltetrazolium chloride staining, the expressions of Bcl-2, Bax, JAK2, STAT3, p-JAK2 and p-STAT3 in ischemic brain tissue were analyzed by Western blotting, and the percentage of caspase-3 positive cells in ischemic brain area was detected by immunofluorescence staining.Results:Compared with sham-operation group, the model group showed significant neurological deficits and cerebral infarction lesions. The expressions of Bax and caspase-3, as well as the phosphorylation levels of JAK2 and STAT3 proteins, were significantly decreased, while the expression of Bcl-2 was significantly up-regulated. Compared with model group, neurological deficits and infarct volume were significantly reduced in OA and inhibitor groups, the expression of Bax, the phosphorylation levels of JAK2 and STAT3, and the percentage of caspase-3 positive cell were significantly decreased, while the expression of Bcl-2 was significantly up-regulated.Conclusion:OA may reduce neuronal apoptosis by inhibiting the activation of the JAK2/STAT3 signaling pathway, and then alleviate I/R injury.
