Rno-microRNA-30c-5p promotes myocardial ischemia reperfusion injury in rats through activating NF-κB pathway and targeting SIRT1
Background: This study aimed to investigate the regulatory effect of rno-microRNA-30c-5p (rno-miR-30c-5p) on myocardial ischemia reperfusion (IR) injury in rats and the underlying molecular mechanisms.
Methods: A rat model of myocardial IR injury was established. The infarct size was detected by 2,3,5-triphenyltetrazolium chloride staining. The pathologic changes of myocardial tissues were detected by hematoxylin-eosin staining. The apoptosis of myocardial cells was measured by TUNEL staining and flow cytometry. The mRNA expression of rno-miR-30c-5p and Sirtuin 1 (SIRT1) was detected by quantitative real-time PCR. The levels of IL-1β, IL-6 and TNF-α were detected by enzyme linked immunosorbent assay. The protein expression of Bax, Bcl-2, caspase-3, p-IκBα, IκBα, p-NF-κB p65, NF-κB p65 and SIRT1 was detected by Western blot. The interaction between rno-miR-30c-5p and SIRT1 was predicted by TargetScan, and further identified by dual luciferase reporter gene and RNA immunoprecipitation assay.
Results: The myocardial IR injury model was successfully established in rats. IR induced the myocardial injury in rats and increased the expression of rno-miR-30c-5p. Overexpression of rno-miR-30c-5p enhanced the inflammation, promoted the apoptosis, and activated NF-κB pathway in IR myocardial cells. SIRT1 was the target gene of rno-miR-30c-5p. Silencing of SIRT1 reversed the effects of rno-miR-30c-5p inhibitor on the apoptosis and NF-κB pathway in IR myocardial cells.
Conclusions: Rno-miR-30c-5p promoted the myocardial IR injury in rats through activating NF-κB pathway and down-regulating SIRT1.
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Posted 14 Apr, 2020
On 08 Apr, 2020
On 07 Apr, 2020
On 07 Apr, 2020
On 01 Apr, 2020
On 08 Mar, 2020
On 07 Mar, 2020
On 07 Mar, 2020
On 03 Mar, 2020
On 02 Mar, 2020
Received 02 Mar, 2020
Invitations sent on 01 Mar, 2020
On 27 Feb, 2020
On 26 Feb, 2020
On 26 Feb, 2020
On 14 Feb, 2020
Received 07 Feb, 2020
Received 07 Feb, 2020
On 24 Jan, 2020
On 24 Jan, 2020
Invitations sent on 23 Jan, 2020
On 22 Jan, 2020
On 21 Jan, 2020
On 21 Jan, 2020
On 22 Dec, 2019
Received 02 Dec, 2019
On 18 Nov, 2019
Received 08 Nov, 2019
On 11 Oct, 2019
Invitations sent on 09 Oct, 2019
On 24 Sep, 2019
On 24 Sep, 2019
On 23 Sep, 2019
On 20 Sep, 2019
Rno-microRNA-30c-5p promotes myocardial ischemia reperfusion injury in rats through activating NF-κB pathway and targeting SIRT1
Posted 14 Apr, 2020
On 08 Apr, 2020
On 07 Apr, 2020
On 07 Apr, 2020
On 01 Apr, 2020
On 08 Mar, 2020
On 07 Mar, 2020
On 07 Mar, 2020
On 03 Mar, 2020
On 02 Mar, 2020
Received 02 Mar, 2020
Invitations sent on 01 Mar, 2020
On 27 Feb, 2020
On 26 Feb, 2020
On 26 Feb, 2020
On 14 Feb, 2020
Received 07 Feb, 2020
Received 07 Feb, 2020
On 24 Jan, 2020
On 24 Jan, 2020
Invitations sent on 23 Jan, 2020
On 22 Jan, 2020
On 21 Jan, 2020
On 21 Jan, 2020
On 22 Dec, 2019
Received 02 Dec, 2019
On 18 Nov, 2019
Received 08 Nov, 2019
On 11 Oct, 2019
Invitations sent on 09 Oct, 2019
On 24 Sep, 2019
On 24 Sep, 2019
On 23 Sep, 2019
On 20 Sep, 2019
Background: This study aimed to investigate the regulatory effect of rno-microRNA-30c-5p (rno-miR-30c-5p) on myocardial ischemia reperfusion (IR) injury in rats and the underlying molecular mechanisms.
Methods: A rat model of myocardial IR injury was established. The infarct size was detected by 2,3,5-triphenyltetrazolium chloride staining. The pathologic changes of myocardial tissues were detected by hematoxylin-eosin staining. The apoptosis of myocardial cells was measured by TUNEL staining and flow cytometry. The mRNA expression of rno-miR-30c-5p and Sirtuin 1 (SIRT1) was detected by quantitative real-time PCR. The levels of IL-1β, IL-6 and TNF-α were detected by enzyme linked immunosorbent assay. The protein expression of Bax, Bcl-2, caspase-3, p-IκBα, IκBα, p-NF-κB p65, NF-κB p65 and SIRT1 was detected by Western blot. The interaction between rno-miR-30c-5p and SIRT1 was predicted by TargetScan, and further identified by dual luciferase reporter gene and RNA immunoprecipitation assay.
Results: The myocardial IR injury model was successfully established in rats. IR induced the myocardial injury in rats and increased the expression of rno-miR-30c-5p. Overexpression of rno-miR-30c-5p enhanced the inflammation, promoted the apoptosis, and activated NF-κB pathway in IR myocardial cells. SIRT1 was the target gene of rno-miR-30c-5p. Silencing of SIRT1 reversed the effects of rno-miR-30c-5p inhibitor on the apoptosis and NF-κB pathway in IR myocardial cells.
Conclusions: Rno-miR-30c-5p promoted the myocardial IR injury in rats through activating NF-κB pathway and down-regulating SIRT1.
Figure 1
Figure 2
Figure 3
Figure 4