Possible role of nitric oxide in hepatic injury secondary to renal ischemia-reperfusion (I/R) injury

Hussein, Abdelaziz M.; Khaled, Hazem K; Seisa, Mohamed O.; Baiomy, Azza; Mohamed, Mie A.; El-Tantawy, Dina; Mahmoud, Amel A; Sheashaa, Hussein; Sobh, Mohamed

doi:10.4149/gpb_2013084

Cited by 3 publications

(2 citation statements)

References 29 publications

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“…Cerebral ischemia-reperfusion (I/R) injury is mainly caused by the restoration of blood perfusion following brain tissue ischemia [ 1 ]. The pathophysiological mechanism of cerebral I/R injury is extremely complex and includes the oxidative stress response, intracellular calcium overload, toxic effects of excitatory amino acids, apoptosis, mitochondrial dysfunction, inflammatory reaction, and so on [ 2 , 3 ]. Cerebral I/R injury can cause apoptosis of hippocampal nerve cells and affect nerve function [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Protection against Hypoxia-Reoxygenation Injury of Hippocampal Neurons by H2S via Promoting Phosphorylation of ROCK2 at Tyr722 in Rat Model

Meng

Chen

et al. 2022

Molecules

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The RhoA-ROCK signaling pathway is associated with the protective effects of hydrogen sulfide (H2S) against cerebral ischemia. H2S protects rat hippocampal neurons (RHNs) against hypoxia-reoxygenation (H/R) injury by promoting phosphorylation of RhoA at Ser188. However, effect of H2S on the phosphorylation of ROCK2-related sites is unclear. The present study was designed to investigate whether H2S can play a role in the phosphorylation of ROCK2 at Tyr722, and explore whether this role mediates the protective effect of H/R injury in RHNs. Prokaryotic recombinant plasmids ROCK2wild-pGEX-6P-1 and ROCK2Y722F-pGEX-6P-1 were constructed and transfected into E. coli in vitro, and the expressed protein, GST-ROCK2wild and GST-ROCK2Y722F were used for phosphorylation assay in vitro. Eukaryotic recombinant plasmids ROCK2Y722-pEGFP-N1 and ROCK2Y722F-pEGFP-N1 as well as empty plasmid were transfected into the RHNs. Western blot assay and whole-cell patch-clamp technique were used to detect phosphorylation of ROCK2 at Tyr722 and BKCa channel current in the RHNs, respectively. Cell viability, leakages of intracellular enzymes lactate dehydrogenase (LDH), and nerve-specific enolase (NSE) were measured. The H/R injury was indicated by decrease of cell viability and leakages of intracellular LDH and NSE. The results of Western blot have shown that NaHS, a H2S donor, significantly promoted phosphorylation of GST-ROCK2wild at Tyr722, while no phosphorylation of GST-ROCK2Y722F was detected. The phosphorylation of ROCK2wild promoted by NaHS was also observed in RHNs. NaHS induced more potent effects on protection against H/R injury, phosphorylation of ROCK2 at Tyr722, inhibition of ROCK2 activity, as well as increase of the BKCa current in the ROCK2Y722-pEGFP-N1-transfected RHNs. Our results revealed that H2S protects the RHNs from H/R injury through promoting phosphorylation of ROCK2 at Tyr722 to inhibit ROCK2 activity and potentially by opening channel currents.

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Section: Introductionmentioning

confidence: 99%

Protection against Hypoxia-Reoxygenation Injury of Hippocampal Neurons by H2S via Promoting Phosphorylation of ROCK2 at Tyr722 in Rat Model

Meng

Chen

et al. 2022

Molecules

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“…NO has many important roles in the liver, including apoptosis inhibition [4,5], liver regeneration [6], and injury prevention [7]. Sumii et al have also shown that NO can increase hepatic function [3].…”

Section: Introductionmentioning

confidence: 99%

Effects of nitric oxide on ammonia decomposition by hepatocytes under shear stress

et al. 2016

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Nitric oxide (NO) and shear stress modulates hepatocyte functions, including ammonia metabolism. This study investigated the simultaneous effects of NO and shear stress on hepatocyte functions. We developed a cell culture device to simultaneously apply NO and shear stress to hepatocytes, and measured changes in ammonia decomposition by hepatocytes in response to changes in NO concentration and shear stress. NO was supplied directly to cells at a constant rate at 0, 0.5, 5, and 25 ppm, and shear stress was either applied at 0.6 Pa or not (static culture). Ammonia decomposition in static culture was higher under all NO loads compared with 0 ppm NO, and was highest under 0.5 ppm NO and decreased under higher NO loads. In the absence of NO load, ammonia decomposition under shear stress was approximately double that in static culture. Under the simultaneous application of NO and shear stress load, ammonia decomposition under 0.5 ppm NO was approximately twice as high as under 0 ppm NO, but was almost the same under 25 ppm NO as under 0 ppm NO. These results indicate that both NO and shear stress enhance ammonia decomposition although the enhancement depends on the NO concentration in their immediate surroundings.

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Exercise Training Attenuates Sympathetic Activation and Oxidative Stress in Diet-Induced Obesity

G¹,

Jy²,

Hx³

et al. 2015

Physiol Res

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It is known that excessive sympathetic activity and oxidative stress are enhanced in obesity. This study aimed to clarify whether exercise training (ET) attenuates sympathetic activation and oxidative stress in obesity. The obesity was induced by high-fat diet (HFD) for 12 weeks. Male Sprague-Dawley rats were assigned to four groups: regular diet (RD) plus sedentary (RD-S), RD plus ET (RD-ET), HFD plus sedentary (HFD-S), and HFD plus ET (HFD-ET). The rats in RD-ET and HFD-ET groups were trained on a motorized treadmill for 60 min/day, five days/week for 8 weeks. The sympathetic activity was evaluated by the plasma norepinephrine (NE) level. The superoxide anion, malondialdehyde and F2-isoprostanes levels in serum and muscles were measured to evaluate oxidative stress. The ET prevented the increases in the body weight, arterial pressure and white adipose tissue mass in HFD rats. The NE level in plasma and oxidative stress related parameters got lower in HFD-ET group compared with HFD-S group. We have found decreased mRNA and protein levels of toll-like receptor (TLR)-2 and TLR-4 by ET in HFD rats. These findings suggest that ET may be effective for attenuating sympathetic activation and oxidative stress in diet-induced obesity.

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Possible role of nitric oxide in hepatic injury secondary to renal ischemia-reperfusion (I/R) injury

Cited by 3 publications

References 29 publications

Protection against Hypoxia-Reoxygenation Injury of Hippocampal Neurons by H2S via Promoting Phosphorylation of ROCK2 at Tyr722 in Rat Model

Protection against Hypoxia-Reoxygenation Injury of Hippocampal Neurons by H2S via Promoting Phosphorylation of ROCK2 at Tyr722 in Rat Model

Effects of nitric oxide on ammonia decomposition by hepatocytes under shear stress

Exercise Training Attenuates Sympathetic Activation and Oxidative Stress in Diet-Induced Obesity

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