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GW24-e2235 Expression and anti-apoptosis role of microRNA-21 in rat myocardium during early ischaemia-reperfusion injury
  1. Yang Qiong,
  2. Yang Kan
  1. Department of Cardiology, The Third Xiangya Hospital of Central South University, Changsha

Abstract

Objectives To observe the expression and anti-apoptosis role of microRNA-21 (miR-21) in rat myocardium during early ischaemia-reperfusion injury (I/R).

Methods Sprague-Dawley rats were randomly divided into five groups: a control group (rats were transfected with rAAV9-ZsGreen by coronary injection); a miR-21group (rats were transfected rAAV9-ZsGreen-pre-miR-21 by coronary injection); a sham group (rats were dealt with open-chest); an I/R group (rats were treated with I/R); an I/R + miR-21 (rats were dealt with I/R after transfected rAAV9-ZsGreen-pre-miR-21 by coronary injection). Realtime-PCR was used to assess the expression level of miR-21; Bax/Bcl-2 and caspase-3 were the key determinants in cell apoptosis, Immunohistochemistry and Western-blot were used to determine the expression of Bax/Bcl-2 and caspase-3.

Results MiR-21 was increased to 4.43 times in miR-21 group than in the control group (P <0.001). MiR-21 was down-regulated in the ischaemia zone after I/R compared with the sham group (P <0.05), but that in the non-ischaemia zone was significantly increased compared with the sham group (P <0.01). MiR-21 expression was decreased in the I/R group than that in the sham group at 1, 2, 6h after I/R (P <0.05), it was up-regulated in the I/R + miR-21 group at the same time point compared with the I/R group (P <0.01). The expression level of Bax/Bcl-2 and caspase-3 was up-regulated in ischaemia zone in the I/R group and I/R + miR-21 group than the sham group (P < 0.05); Compared with the I/R group, the expression of Bax/Bcl-2 and caspase-3 was down-regulated in ischaemia zone in the I/R + miR-21 group (P < 0.05).

Conclusions The expression of miR-21 is down-regulated and cell apoptosis is increased in rat myocardium during early ischaemia-reperfusion injury, myocardial cell apoptosis may be alleviated by over-expressed miR-2.

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