Dataset Information

Hydrogen-rich saline alleviates inflammation and apoptosis in myocardial I/R injury via PINK-mediated autophagy.

ABSTRACT: Ischemia/reperfusion (I/R)‑induced inflammatory reaction is one of the most important elements in myocardial I/R injury. In addition, autophagy serves an important role in normal cardiac homeostasis, and obstructions to the autophagy process lead to severe consequences for the heart. Hydrogen exerts an effective therapeutic role in numerous diseases associated with I/R injury via its anti‑inflammation, anti‑apoptosis and anti‑oxidative properties. Therefore, the present study investigated the effect of hydrogen on the myocardial inflammation response and apoptosis in myocardial ischemic/reperfusion (MI/R) injury, and further explored the mechanism of PTEN‑induced kinase 1 (PINK1)/Parkin‑induced mitophagy in the protection of hydrogen on MI/R injury. MI/R injury was performed by surgical ligation of the left coronary artery in vivo and H9C2 cell injury was performed by hypoxia/reoxygenation (H/R) in vitro. Hydrogen‑rich saline was administered twice through intraperitoneal injection at a daily dose of 10 ml/kg following the operation in the in vivo model, and hydrogen‑rich medium culture was used for cells instead of normal medium in vitro. The infarction size of hearts, the levels of creatinine kinase‑muscle/brain (CK‑MB) and cardiac troponin I (cTnI), cardiac function, cell viability and lactate dehydrogenase (LDH) release, levels of cytokines, apoptosis and the expression of autophagy‑associated proteins were detected in the different treatment groups in vivo and in vitro. The results demonstrated that treatment with hydrogen improved the myocardial infarction size of hearts, cardiac function, apoptosis and cytokine release following MI/R in rats. In vitro, hydrogen improved cell viability and LDH release following hypoxia/reoxygenation in myocardial cells. In addition, it was demonstrated that hydrogen exerted an anti‑inflammatory and anti‑apoptotic effect in myocardial cells induced by H/R via PINK1/Parkin mediated autophagy. These results suggested that hydrogen‑rich saline alleviated the inflammation response and apoptosis induced by MI/R or H/R in vivo or in vitro, and that hydrogen‑rich saline contributed to the increased expression of proteins associated with autophagy. In summary, the present study indicated that treatment with hydrogen‑rich saline improved the inflammatory response and apoptosis in MI/R via PINK1/Parkin‑mediated mitophagy.

SUBMITTER: Yao L

PROVIDER: S-EPMC6657957 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Purpose: Acute kidney injury (AKI) is a prominent risk factor for the development of chronic kidney disease (CKD). To date, the related mechanism and effective therapy have not been rigorously explored. The present study aims to investigate the reno-protection of hydrogen-rich saline (HRS) against ischemia/reperfusion (IR)-induced AKI. Methods: Adult male C57 mice were randomly allocated into three groups: Sham, IR, IR+HRS. Renal IR injury model was generated via 35 min occlusion of bilateral kidney pedicles, and then, mice were administered with different treatments intraperitoneally in various groups. After 14- or 28-day treatment, mice were perfused and the kidneys were collected following reperfusion. Many proteins were detected by western blots, including renal fibrotic proteins [a-smooth muscle actin (a-SMA), collagen I (Col I)], Klotho, the methylation of Klotho, damage-regulated autophagy modulator (Beclin-1), and microtubule-associated protein light 3-II (LC3-II). Finally, the levels of serum blood urea nitrogen (BUN) and creatinine (Cr) were measured to investigate the renal function. Results: Histological data showed that the HRS treatment significantly decreased the fibrosis in renal tissues when compared with the IR group, and both of BUN and Cr were lower in the HRS group than IR group (8.9 ± 0.6 vs. 9.9 ± 0.1 mmol/l, 51 ± 6.5 vs. 60 ± 5.8 μmol/l) (P < 0.05). The expression of fibrotic markers, a-SMA and Col I, showed a robust increase in IR injury models than the Sham group, which was consistent with the result of Trichrome staining. However, the levels of a-SMA and Col I expression were sharply decreased in the IR+HRS group (P < 0.05). IR injury also enhanced LC3-II and Beclin-1 expression, but decreased Klotho level. The Klotho level was alleviated by HRS, but LC3-II and Beclin-1 were starkly enhanced in HRS group (P < 0.05). Conclusion: HRS showed a protective effect in the prevention of renal injury and could inhibit renal fibrosis after IR injury in mice. This role of HRS might be exerted via retaining Klotho expression and activating autophagy in the kidney.

Dataset Information

Hydrogen-rich saline alleviates inflammation and apoptosis in myocardial I/R injury via PINK-mediated autophagy.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets