Inactivated pseudomonas�aeruginosa protects against myocardial ischemia reperfusion injury via Nrf2 and HO‑1

Abstract

The current study investigated the protective effects of inactivated pseudomonas aeruginosa (IPA) on myocardial ischemia reperfusion injury (MIR/I) and the mechanisms governing this interaction. Left anterior descending coronary artery ligation was performed on rats for 30 min and reperfusion was performed for a subsequent 2 h. Rat hearts were obtained and the myocardial infarction area was determined using nitroblue tetrazolium. Myocardial cell apoptosis was determined using flow cytometry. Malondialdehyde (MDA) content, lactate dehydrogenase (LDH) activity, superoxide dismutase (SOD) activity and catalase (CAT) activities were assayed using the corresponding kits. Additionally, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) were assayed using western blot and immunofluorescence analysis. When compared with the model group, the results of IPA treatment revealed improved heart function, reduced myocardial infarction area and reduced endothelial cell apoptosis, which led to decreased LDH and MDA levels, and increased SOD and CAT levels in serum, and decreased LDH and MDA levels and increased SOD and CAT in myocardial tissues. Moreover, increased Nrf2 and HO-1 expression levels in the myocardial tissues were also observed at all concentrations of IPA. It was concluded that IPA pretreatment ameliorated MIR/I and reduced endothelial apoptosis and oxidative stress via the Nrf2/HO-1 pathway.

APPL1 ameliorates myocardial ischemia‑reperfusion injury by regulating the AMPK signaling pathway

“…Nrf2 could directly regulate the promoter activities of HO-1, a vital antioxidase that is involved in myocardial ischemia reperfusion injury. Compared with those in the control group, the expression levels of NRF2 and HO-1 (30) were significantly reduced by H/R treatment and these effects were significantly recovered by APPL1 overexpression (Fig. 7).…”

Heat-Killed Lacticaseibacillus paracasei Ameliorated UVB-Induced Oxidative Damage and Photoaging and Its Underlying Mechanisms

“…Correlation analysis showed that Sirt1 protein expression was positively correlated with PGC-1α and N-Nrf2 protein expression (As shown in Table S2 ), indicating that the increased antioxidant enzyme activities by PL may be related to Sirt1/PGC-1α/Nrf2 signaling in NHDF cells. Moreover, a study from rats showed that inactivated pseudomonas aeruginosa could protect against oxidative stress through enhancing SOD and CAT activities relating to the Nrf2 signaling pathway in the heart [ 59 ]. It was reported that exopolysaccharides produced by Lactobacillus rhamnosus GG could alleviate oxidative damage through increasing SOD activity relating to the Nrf2 signaling pathway in intestinal porcine epithelial cells [ 60 ].…”

Protective Effect of Blood Cora Polysaccharides on H9c2 Rat Heart Cells Injury Induced by Oxidative Stress by Activating Nrf2/HO-1 Signal Pathway

“…Under normal physiological status, the body contains relatively low amounts of serum LDH, and LDH within the cells is released in large amounts only after cell membrane injury occurs. As the major endogenous antioxidant in vivo , SOD removes excess oxygen radicals in vivo to reduce mitochondrial injury and maintain cell stability ( 30 ). In the BCP treatment group, the LDH content in the supernatant and MDA in cells significantly decreased, and the SOD in cells significantly increased, compared with that of the model group.…”