title: Cardioprotective effect of Aralia elata polysaccharide on myocardial ischemic reperfusion (IR) injury in rats.
abstract: Based on the previous studies revealing antioxidant activities of a water-soluble polysaccharide (AEP-w1) from the root bark of Aralia elata, the present study was designed to determine if chronic administration of AEP-w1 could reduce ischemic reperfusion (IR) induced myocardial injury. Wistar rats were given three different doses of AEP-w1 (50, 100 and 200mg/kg/day) or vehicle for 30 days, after which myocardial IR injury was induced by the occlusion of left anterior descending (LAD) coronary artery for 45min followed by 60min of reperfusion. Pretreatment with AEP-w1 not only enhanced the serum levels of total antioxidant capacity (T-AOC), superoxide dismutase (SOD) and glutathione (GSH), but also decreased the serum malondialdehyde (MDA) level in rats suffering IR injury. Consistent with this observation, AEP-w1 treatment also restored the myocardial antioxidant status evidenced by increased SOD, catalase (CAT) and glutathione (GSH) and decreased thiobarbituric acid reactive substances (TBARS) as compared to the IR model group. Furthermore, the elevated level of pro-inflammatory cytokines, such as TNF-α and IL-6, and decreased level of anti-inflammatory cytokine IL-10 in vehicle-treated IR rats was reversed by pretreatment with AEP-w1. In addition, AEP-w1 prevented myocardial cell from apoptosis in mice subjected to IR injury. These findings revealed that cardioprotective effect of AEP-w1 was achieved likely through improving endogenous antioxidants, regulating the inflammation response and suppressing myocardial cell apoptosis.
authors.affiliation: Department of Cardiology, Tangdu Hospital, The Fourth Military Medical University, Xi'an 710038, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Zhang
authors.forename: Haiyan
authors.initials: H
authors.lastname: Wang
authors.forename: Qiangsun
authors.initials: Q
authors.lastname: Zheng
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000302:isolation & purification / Q000494:pharmacology*; D027983:Aralia / Q000737:chemistry*; D002316:Cardiotonic Agents / Q000302:isolation & purification / Q000494:pharmacology*; D002374:Catalase / Q000097:blood; D005978:Glutathione / Q000819:agonists / Q000097:blood; D016753:Interleukin-10 / Q000819:agonists / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D007770:L-Lactate Dehydrogenase / Q000037:antagonists & inhibitors / Q000097:blood; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000188:drug therapy*; D018517:Plant Roots / Q000737:chemistry*; D011134:Polysaccharides / Q000302:isolation & purification / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000097:blood; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000097:blood; D000093242:Interleukin-6 Inhibitors
chemical_list: D000975:Antioxidants; D002316:Cardiotonic Agents; D002374:Catalase; D005978:Glutathione; D016753:Interleukin-10; D015850:Interleukin-6; D007770:L-Lactate Dehydrogenase; D011134:Polysaccharides; D013482:Superoxide Dismutase; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha; D000093242:Interleukin-6 Inhibitors