Perillyl alcohol protects human renal tubular epithelial cells from hypoxia/reoxygenation injury via inhibition of ROS, endoplasmic reticulum stress and activation of PI3K/Akt/eNOS pathway

Xu, Yancheng; Wang, Wan-Tie; Jin, Keke; Zhu, Qifan; Lin, Hui; Xie, Minye; Wang, Dexuan

doi:10.1016/j.biopha.2017.08.129

Cited by 28 publications

(16 citation statements)

References 28 publications

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“…Understanding the detailed mechanism of I/R injury is crucial for novel therapeutic and prevention approaches. Growing evidence focused on the basic pathophysiology of I/R injury reveal that the increasing ROS production and cell death pathways are particularly important for the I/R injury . During I/R period, the content of ROS is dramatically increased due to the excessive generation of ROS and lower concentration of antioxidative agents .…”

Section: Discussionmentioning

confidence: 99%

Cryptotanshinone inhibits hypoxia/reoxygenation‐induced oxidative stress and apoptosis in renal tubular epithelial cells

Zhu

Wang

Yang

2019

J of Cellular Biochemistry

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Cryptotanshinone (CTS), an active component extracted from the root of Salvia miltiorrhiza Bunge, was reported to attenuate hepatic ischemia/reperfusion (I/R) injury. However, its protective effect against renal I/R injury remains unclear. In this study, the role of CTS in renal I/R injury in vitro and its possible mechanism were investigated. Our results showed that CTS improved cell viability in HK-2 cells exposed to hypoxia/reoxygenation (H/R). CTS also inhibited the H/Rmediated production of reactive oxygen species, as well as increased the activities of superoxide dismutase and catalase in H/R-stimulated HK-2 cells. In addition, CTS dramatically attenuated the induction of bax expression and caspase-3 activity and alleviated the reduction of bcl-2 expression in HK-2 cells cultured with H/R. Furthermore, CTS activated the levels of p-PI3K and p-Akt in H/R-injured HK-2 cells; meanwhile, the renal protective activity of CTS was inhibited by the inhibitor of the (phosphatidylinositol 3 kinase/protein kinase B) PI3K/Akt pathway (LY294002). These findings indicate that CTS can ameliorate renal I/R injury in vitro partly through regulating the PI3K/Akt pathway. K E Y W O R D S acute kidney injury, cryptotanshinone, hypoxia/reoxygenation, ischemia/reperfusion injury, oxidative stress J Cell Biochem. 2019;120:13354-13360. wileyonlinelibrary.com/journal/jcb 13354 |

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Section: Discussionmentioning

confidence: 99%

Cryptotanshinone inhibits hypoxia/reoxygenation‐induced oxidative stress and apoptosis in renal tubular epithelial cells

Zhu

Wang

Yang

2019

J of Cellular Biochemistry

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“…Pi3K/aKT pathway activation is an endogenous regulatory mechanism that promotes cell survival in response to harmful external stimuli. notably, numerous studies suggest that the Pi3K/aKT pathway plays a pivotal role in the pathological process of renal i/r injury, in which inhibition of erS-related apoptosis is an important mechanism (43,44). Zhang et al (26) have reported that Pi3K/aKT signaling inhibits i/r injury by suppressing erS, thus reducing GrP78, cHoP, and caspase-12 levels and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Nobiletin alleviates ischemia/reperfusion injury in the kidney by activating PI3K/AKT pathway

et al. 2020

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recent studies have demonstrated that nobiletin (NOB) displays anti-oxidative and anti-apoptotic efficacies against multiple pathological insults. However, the potential effects of noB on the injury caused by ischemia and reperfusion (i/r) in the kidney remain undetermined. in the present study, i/r injury was elicited by right kidney removal and left renal pedicel clamping for 45 min, followed by reperfusion for 24 h. noB was added at the start of reperfusion. Histological examination, detection of biomarkers in plasma, and measurement of apoptosis induced by endoplasmic reticulum stress (erS) were used to evaluate renal injury. additionally, the Pi3K/aKT inhibitor lY294002 was also used in mechanistic experiments. NOB pre-treatment significantly reduced renal damage caused by i/r injury, as indicated by decreased serum levels of creatine, blood urea nitrogen and tubular injury scores. Furthermore, noB inhibited elevated erS-associated apoptosis, as evidenced by reduced apoptotic rates and erS-related signaling molecules (such as, c/eBP homologous protein, caspase-12 and glucose-regulated protein of 78 kda). noB increased phosphorylation of proteins in the Pi3K/aKT pathway. The inhibition of Pi3K/aKT signaling with pharmacological inhibitors could reverse the beneficial effects of NOB during renal i/r insult. in conclusion, noB pre-treatment may alleviate i/r injury in the kidney by inhibiting reactive oxygen species production and erS-induced apoptosis, partly through the Pi3K/aKT signaling pathway.

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“…For the assessment of reactive oxygen species (ROS), DCF-DA (Thermo Scientific) was used as an ROS probe, as previously described (16). After different treatments, the cells were incubated with 5 µM DCF-DA for 30 min at 37°C.…”

Section: Methodsmentioning

confidence: 99%

miR‑455 targets FABP4 to protect human endometrial stromal cells from cytotoxicity induced by hydrogen peroxide

et al. 2019

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Oxidative stress and dysregulation of antioxidant systems are associated with various complications in pregnancy. Endometriosis is a common gynecologic disease that affects women of reproductive age. Recent studies have indicated that oxidative stress may be involved in the pathophysiology of endometriosis. It has been reported that microRNAs can regulate the cellular response to oxidative stress, and mounting evidence indicates that fatty acid binding protein 4 (FABP4) plays an essential role in the regulation of systemic redox capacity. In the present study, we demonstrated that miR-455 is a putative FABP4-targeting miRNA. A luciferase activity assay revealed that miR-455 can successfully bind to the 3′-UTR of FABP4. Overexpression of miR-455 led to the downregulation of FABP4 at both the mRNA and protein levels in a human endometrial stromal cell line. Then, the roles of miR-455 and FABP4 in oxidative stress induced by hydrogen peroxide (H2O2) in human endometrial stromal cells were examined. We found that ectopic expression of miR-455 protected cells from damage caused by H2O2. Further investigation found that forced expression of miR-455 reduced the level of reactive oxygen species (ROS) and malondialdehyde (MDA), while the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were promoted. Silencing of FABP4 also generated cytoprotective effects against H2O2 in human endometrial stromal cells. Moreover, overexpression FABP4 abrogated the miR-455-mediated antioxidative stress effects in cells. Taken together, we propose that miR-455 protects human endometrial stromal cells from oxidative stress at least partly via regulation of FABP4.

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Perillyl alcohol protects human renal tubular epithelial cells from hypoxia/reoxygenation injury via inhibition of ROS, endoplasmic reticulum stress and activation of PI3K/Akt/eNOS pathway

Cited by 28 publications

References 28 publications

Cryptotanshinone inhibits hypoxia/reoxygenation‐induced oxidative stress and apoptosis in renal tubular epithelial cells

Cryptotanshinone inhibits hypoxia/reoxygenation‐induced oxidative stress and apoptosis in renal tubular epithelial cells

Nobiletin alleviates ischemia/reperfusion injury in the kidney by activating PI3K/AKT pathway

miR‑455 targets FABP4 to protect human endometrial stromal cells from cytotoxicity induced by hydrogen peroxide

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