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. 2021 Dec;12(1):5529-5539.
doi: 10.1080/21655979.2021.1965696.

Argon inhibits reactive oxygen species oxidative stress via the miR-21-mediated PDCD4/PTEN pathway to prevent myocardial ischemia/reperfusion injury

Hong Qi  1 , Jiancheng Zhang  1 , You Shang  1 , Shiying Yuan  1 , Chunqing Meng  2
Affiliations

Argon inhibits reactive oxygen species oxidative stress via the miR-21-mediated PDCD4/PTEN pathway to prevent myocardial ischemia/reperfusion injury

Hong Qi et al. Bioengineered. 2021 Dec.

Abstract

The objective of this study was to explore the effect of argon preconditioning on myocardial ischemia reperfusion (MI/R) injury and its mechanism. Cardiomyocytes H2C9 were pre-treated with 50% argon, and a cell model of oxygen-glucose deprivation (OGD) was established. CCK-8 and cytotoxicity detection kits were used to detect cell viability and lactate dehydrogenase (LDH) release. The miR-21 expression was detected using quantitative real-time polymerase chain reaction. Western blot analysis was performed to detect the expression of programmed cell death protein 4 (PDCD4) and homologous phosphatase and tensin homolog (PTEN) proteins. The levels of inflammatory factors (IL-1β, IL-6, and IL-8) and oxidative stress factors (reactive oxygen species ROS], malondialdehyde [MDA], and superoxide dismutase [SOD]) were measured using an enzyme-linked immunosorbent assay. The effect of argon on cell apoptosis was detected using flow cytometry. Argon increased the proliferation of cardiomyocytes induced by OGD, decreased the release of LDH in cell culture medium, increased miR-21 expression in cells, decreased the expression of miR-21 target proteins PDCD4 and PTEN, decreased the levels of inflammatory factors (interleukin-1β [IL-1β], interleukin-6 [IL-6], and interleukin-8 [IL-8]) and oxidative stress factors (ROS and MDA), increased the SOD content, and decreased the cell apoptosis rate. Our results suggest that argon preconditioning inhibited the PDCD4/PTEN pathway via miR-21, thereby inhibiting ROS oxidative stress and preventing MI/R injury.

Keywords: Argon; PDCD4/PTEN pathway; ROS oxidative; miR-21.

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Conflict of interest statement

No potential conflict of interest was reported by the author(s).

Figures

Figure 1.
Figure 1.
Effect of argon on the viability of OGD-induced cells. **P < 0.01, ***P < 0.001 vs. normal group; ##P < 0.01, ###P < 0.001 vs. short-term hypoxia group; ΔΔΔP < 0.001 vs. long-term hypoxia group
Figure 2.
Figure 2.
Effect of argon on LDH release in OGD-induced cells. ***P < 0.001 vs. normal group; ###P < 0.001 vs. short-term hypoxia group; ΔΔΔP < 0.001 vs. long-term hypoxia group
Figure 3.
Figure 3.
Effect of argon on miR-21 expression in OGD-induced cells. **P < 0.01, ***P < 0.001 vs. normal group; ##P < 0.01 vs. short-term hypoxia group; ΔΔP < 0.01 vs. long-term hypoxia group
Figure 4.
Figure 4.
Effect of argon on the expression of PDCD4 and PTEN (miR-21 target proteins) in OGD-induced cells. ***P < 0.001 vs. normal group; ###P < 0.001 vs. short-term hypoxia group; ΔΔΔP < 0.001 vs. long-term hypoxia group
Figure 5.
Figure 5.
Effects of argon on the contents of inflammatory factors (IL1β, IL-6, and IL-8) and oxidative stress factors (ROS, MDA, and SOD) in OGD-induced cells. *P < 0.05, **P < 0.01, ***P < 0.001 vs. normal group; #P < 0.05, ##P < 0.01 vs. short-term hypoxia group; ###P < 0.001 vs. short-term hypoxia group; ΔΔP < 0.01, ΔΔΔP < 0.001 vs. long-term hypoxia group
Figure 6.
Figure 6.
Effect of argon on the apoptosis of OGD-induced cells. *P < 0.05, **P < 0.01, ***P < 0.001 vs. normal group; ###P < 0.001 vs. short-term hypoxia group; ΔΔΔP < 0.001 vs. long-term hypoxia group
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