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Neuroprotection of Osthole against Cerebral Ischemia/Reperfusion Injury through an Anti-apoptotic Pathway in Rats.
Biol Pharm Bull. 2016; 39(3):336-42.BP

Abstract

Cerebral ischemia/reperfusion (I/R) injury is a major cause of acute brain injury. The pathogenetic mechanisms underlying I/R injury involve apoptosis, inflammation and oxidative stress. Osthole-a plant coumarin compound-has been reported to protect against focal cerebral I/R-induced injury in rats. However, the mechanism remains unknown. Here we hypothesize that osthole acts through inhibition of apoptosis during focal cerebral I/R injury in rats. We induced cerebral I/R injury by middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion. We randomly assigned 60 rats to three groups (20 rats per group): sham-operated, vehicle-treated I/R, and osthole-treated I/R. We treated rats intraperitoneally with osthole (40 mg/kg) or vehicle 30 min before cerebral ischemia. We harvested the brains for infarct volume, brain water content, histological changes and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) staining as well as cleaved caspase-3, bax, and bcl-2 levels 24 h after reperfusion. Osthole treatment significantly attenuated cerebral dysfunction and histologic damage induced by I/R injury. Moreover, osthole-treated rats had a dramatic decrease in apoptotic neuronal cells along with a decrease in bax and cleaved caspase-3. The bcl-2 levels increased. Osthole treatment protects the brain from cerebral I/R injury by suppressing cell apoptosis. Thus, osthole may represent a novel practical strategy to prevent cerebral I/R injury.

Authors+Show Affiliations

Department of Radiology, First Affiliated Hospital of Xi'an Jiaotong University.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

26934926

Citation

Li, Kang, et al. "Neuroprotection of Osthole Against Cerebral Ischemia/Reperfusion Injury Through an Anti-apoptotic Pathway in Rats." Biological & Pharmaceutical Bulletin, vol. 39, no. 3, 2016, pp. 336-42.
Li K, Ding D, Zhang M. Neuroprotection of Osthole against Cerebral Ischemia/Reperfusion Injury through an Anti-apoptotic Pathway in Rats. Biol Pharm Bull. 2016;39(3):336-42.
Li, K., Ding, D., & Zhang, M. (2016). Neuroprotection of Osthole against Cerebral Ischemia/Reperfusion Injury through an Anti-apoptotic Pathway in Rats. Biological & Pharmaceutical Bulletin, 39(3), 336-42. https://doi.org/10.1248/bpb.b15-00699
Li K, Ding D, Zhang M. Neuroprotection of Osthole Against Cerebral Ischemia/Reperfusion Injury Through an Anti-apoptotic Pathway in Rats. Biol Pharm Bull. 2016;39(3):336-42. PubMed PMID: 26934926.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotection of Osthole against Cerebral Ischemia/Reperfusion Injury through an Anti-apoptotic Pathway in Rats. AU - Li,Kang, AU - Ding,Dun, AU - Zhang,Ming, PY - 2016/3/4/entrez PY - 2016/3/5/pubmed PY - 2016/12/15/medline SP - 336 EP - 42 JF - Biological & pharmaceutical bulletin JO - Biol Pharm Bull VL - 39 IS - 3 N2 - Cerebral ischemia/reperfusion (I/R) injury is a major cause of acute brain injury. The pathogenetic mechanisms underlying I/R injury involve apoptosis, inflammation and oxidative stress. Osthole-a plant coumarin compound-has been reported to protect against focal cerebral I/R-induced injury in rats. However, the mechanism remains unknown. Here we hypothesize that osthole acts through inhibition of apoptosis during focal cerebral I/R injury in rats. We induced cerebral I/R injury by middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion. We randomly assigned 60 rats to three groups (20 rats per group): sham-operated, vehicle-treated I/R, and osthole-treated I/R. We treated rats intraperitoneally with osthole (40 mg/kg) or vehicle 30 min before cerebral ischemia. We harvested the brains for infarct volume, brain water content, histological changes and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) staining as well as cleaved caspase-3, bax, and bcl-2 levels 24 h after reperfusion. Osthole treatment significantly attenuated cerebral dysfunction and histologic damage induced by I/R injury. Moreover, osthole-treated rats had a dramatic decrease in apoptotic neuronal cells along with a decrease in bax and cleaved caspase-3. The bcl-2 levels increased. Osthole treatment protects the brain from cerebral I/R injury by suppressing cell apoptosis. Thus, osthole may represent a novel practical strategy to prevent cerebral I/R injury. SN - 1347-5215 UR - https://www.unboundmedicine.com/medline/citation/26934926/Neuroprotection_of_Osthole_against_Cerebral_Ischemia/Reperfusion_Injury_through_an_Anti_apoptotic_Pathway_in_Rats_ L2 - https://dx.doi.org/10.1248/bpb.b15-00699 DB - PRIME DP - Unbound Medicine ER -