Ca+2 Concentrations are Key Determinants of Ischemia-Reperfusion-Induced Apoptosis: Significance for the Molecular Mechanism of Bcl-2 Action

被引：18

作者：

Chattopadhyay, Pronobesh ^{[1
,2
]}

Chaudhury, Pallab ^{[3
]}

Wahi, Arun Kumar ^{[2
]}

机构：

[1] Birla Inst Technol & Sci, Pilani 333031, Rajasthan, India

[2] IFTM, Coll Pharm, Lodhipur Rajput 244001, Moradabad, India

[3] Indian Vet Res Inst, Natl Biotechnol Ctr, Izatnagar 244112, Uttar Pradesh, India

来源：

APPLIED BIOCHEMISTRY AND BIOTECHNOLOGY | 2010年 / 160卷 / 07期

关键词：

Ca+2; Bcl-2; Apoptosis; Ischemia reperfusion; CELLS; LIVER;

D O I：

10.1007/s12010-009-8761-2

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The mechanism of action of the anti-apoptotic oncogene Bcl-2 and Ca+2 regulation in ischemia-reperfusion injury is still obscure. In this present study, we investigated mitochondrial Ca+2 overloads and mechanism of action of Bcl-2. Eighteen Wistar rats were divided into sham-operated control group (I) (n=6), ischemia and reperfusion group (II) (n=6), and amlodipine-treated group (1 mg kg(-1) body weight/daily by oral route for 7 days before inducing ischemia-reperfusion maneuver) (III) (n=6). Rats were subjected to 1 h of hepatic ischemia followed by 3-h reperfusion. Mitochondrial Ca2+ content was determined and damage was confirmed by transmission electron microscopy. Decrease of mitochondrial Ca+2 level is related to reduction of apoptosis and cellular changes, viz. increased Bcl-2 expression followed by reduction in secondary endoplasmic reticulum, whereas ischemia/reperfusion group shows overloading Ca+2 ions and decrease in Bcl-2 expression as compared to sham-operated rats. Thus, Bcl-2-dependent reduction of Ca+2 is an important component of the anti-apoptotic program in ischemia-reperfusion injury.

引用

页码：1968 / 1977

页数：10

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