Resveratrol Protects Against Post-Contrast Acute Kidney Injury in Rabbits With Diabetic Nephropathy

Wang, Yongfang; Wang, Bin; Qi, Xun; Zhang, Xin; Kawaguchi, Ren

doi:10.3389/fphar.2019.00833

Cited by 31 publications

(28 citation statements)

References 40 publications

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“…Resveratrol has been shown to decrease intracellular reactive oxygen species levels via downregulation of the nicotinamide adenine dinucleotide phosphate oxidase subunits NOX1 and NOX4 in high glucose-treated human tubular epithelial cells (HK2) [ 27 ]. In addition, resveratrol has been demonstrated to ameliorate post-contrast acute kidney injury (PC-AKI) following diabetic nephropathy in vivo and in vitro [ 28 ]. Moreover, resveratrol reduced the expression levels of IL-1β and cell apoptosis in a PC-AKI model [ 10 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of resveratrol on the inflammatory response and renal injury in hyperuricemic rats

Ben-xi

Zheng

et al. 2021

Nutr Res Pract

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BACKGROUND/OBJECTIVES Hyperuricemic nephropathy is a common cause of acute kidney injury. Resveratrol can ameliorate kidney injury, but the explicit mechanism remains unclear. We investigated the effects of resveratrol on the inflammatory response and renal injury in hyperuricemic rats. MATERIALS/METHODS A rat model of hyperuricemic nephropathy was established by the oral administration of a mixture of adenine and potassium oxinate. Biochemical analysis and hematoxylin and eosin staining were performed to assess the rat kidney function. Enzyme-linked immunosorbent assays were performed to evaluate the immune and oxidative responses. RESULTS The expression levels of urine albumin and β2-microglobulin were significantly decreased after resveratrol treatment. In addition, the levels of serum creatinine and uric acid were significantly decreased in the resveratrol groups, compared with the control group. The levels of proinflammatory factors, such as interleukin-1β and tumor necrosis factor-α, in kidney tissue and serum were also increased in the hyperuricemic rats, and resveratrol treatment inhibited their expression. Moreover, the total antioxidant capacity in kidney tissue as well as the superoxide dismutase and xanthine oxidase levels in serum were all decreased by resveratrol treatment. CONCLUSIONS Resveratrol may protect against hyperuricemic nephropathy through regulating the inflammatory response.

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Section: Discussionmentioning

confidence: 99%

Effects of resveratrol on the inflammatory response and renal injury in hyperuricemic rats

Ben-xi

Zheng

et al. 2021

Nutr Res Pract

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“…These results reveal that high glucose-induced changes on autophagy play an important role in diabetes-associated podocyte injury. However, in diabetic kidney disease, other than autophagy, other mechanisms, such as antioxidant and anti-inflammation effects, have been suggested to offer renal protection (Sun et al, 2019 ; Wang et al, 2019 ). Therefore, there is a need to investigate the involvement of other mechanisms in regulating the renoprotective function of miR-150-5p.…”

Section: Discussionmentioning

confidence: 99%

Silencing of miR-150-5p Ameliorates Diabetic Nephropathy by Targeting SIRT1/p53/AMPK Pathway

et al. 2021

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Diabetic nephropathy (DN) is a common complication of diabetes and an important cause of end-stage renal disease. Increasing evidence suggests that microRNAs (miRNAs) regulate the development of DN. In a preliminary study, high levels of miR-150-5p were detected in the serum and urine of patients with DN. Consequently, we investigated the effect and mechanism of action of miR-150-5p in DN in vitro and in vivo. Our results showed that inhibition of miR-150-5p reversed high glucose-induced podocyte injury and Streptozocin (STZ)-induced diabetic nephropathy in mice. Further analysis revealed that miR-150-5p targeted the 3′ untranslated region (UTR) of sirtuin 1 (SIRT1), consequently decreasing SIRT1 levels in podocytes. Importantly, we found that the silencing of miR-150-5p promoted the interaction between SIRT1 and p53, causing the suppression of p53 acetylation in podocytes and kidney tissue. This resulted in the stimulation of AMP-activated protein kinase (AMPK)-dependent autophagy. In conclusion, our study demonstrated that the silencing of miR-150-5p played a reno-protective role in DN mice through targeting SIRT1.

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“…The cultures were then placed in an incubator chamber containing a mixed gas of 5% CO 2 and 95% N 2 at 37°C for 3 h. The neuronal cells in the control group were placed in glucose-containing DMEM medium for the same period of time. After 3 h, the neuronal cells were returned to normal oxygen conditions and reperfused for 24 h. For the LEVtreated neuronal cells, the drug was added to the cells at a final concentration of 1 mmol/L at the beginning of OGD and replenished immediately after reperfusion (Wang et al, 2019). Neuronal cells were seeded in 6-well plates at a density of 1 × 10 5 cells/well.…”

Section: Flow Cytometry Analysis Of Cell Apoptosismentioning

confidence: 99%

Neuroprotective and Angiogenesis Effects of Levetiracetam Following Ischemic Stroke in Rats

et al. 2021

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Objective: The present study explored whether levetiracetam (LEV) could protect against experimental brain ischemia and enhance angiogenesis in rats, and investigated the potential mechanisms in vivo and in vitro.Methods: The middle cerebral artery was occluded for 60 min to induce middle cerebral artery occlusion (MCAO). The Morris water maze was used to measure cognitive ability. The rotation test was used to assess locomotor function. T2-weighted MRI was used to assess infarct volume. The neuronal cells in the cortex area were stained with cresyl purple. The anti-inflammatory effects of LEV on microglia were observed by immunohistochemistry. Enzyme-linked immunosorbent assays (ELISA) were used to measure the production of pro-inflammatory cytokines. Western blotting was used to detect the levels of heat shock protein 70 (HSP70), vascular endothelial growth factor (VEGF), and hypoxia-inducible factor-1α (HIF-1α) in extracts from the ischemic cortex. Flow cytometry was used to observe the effect of LEV on neuronal cell apoptosis.Results: LEV treatment significantly increased the density of the surviving neurons in the cerebral cortex and reduced the infarct size (17.8 ± 3.3% vs. 12.9 ± 1.4%, p < 0.01) after MCAO. Concurrently, the time required to reach the platform for LEV-treated rats was shorter than that in the saline group on day 11 after MCAO (p < 0.01). LEV treatment prolonged the rotarod retention time on day 14 after MCAO (84.5 ± 6.7 s vs. 59.1 ± 6.2 s on day 14 compared with the saline-treated groups, p < 0.01). It also suppressed the activation of microglia and inhibited TNF-α and Il-1β in the ischemic brain (135.6 ± 5.2 pg/ml vs. 255.3 ± 12.5 pg/ml, 18.5 ± 1.3 pg/ml vs. 38.9 ± 2.3 pg/ml on day 14 compared with the saline-treated groups, p < 0.01). LEV treatment resulted in a significant increase in HIF-1α, VEGF, and HSP70 levels in extracts from the ischemic cerebral cortex. At the same time, LEV reduced neuronal cell cytotoxicity and apoptosis induced by an ischemic stroke (p < 0.01).Conclusion: LEV treatment promoted angiogenesis and functional recovery after cerebral ischemia in rats. These effects seem to be mediated through anti-inflammatory and antiapoptotic activities, as well as inducing the expression of HSP70, VEGF, and HIF-1α.

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Resveratrol Protects Against Post-Contrast Acute Kidney Injury in Rabbits With Diabetic Nephropathy

Cited by 31 publications

References 40 publications

Effects of resveratrol on the inflammatory response and renal injury in hyperuricemic rats

Effects of resveratrol on the inflammatory response and renal injury in hyperuricemic rats

Silencing of miR-150-5p Ameliorates Diabetic Nephropathy by Targeting SIRT1/p53/AMPK Pathway

Neuroprotective and Angiogenesis Effects of Levetiracetam Following Ischemic Stroke in Rats

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