Biological Membrane-Packed Mesenchymal Stem Cells Treat Acute Kidney Disease by Ameliorating Mitochondrial-Related Apoptosis

This study was designed to investigate the protective effect of curcumin against d-galactose (d-gal)-induced premature ovarian failure (POF) in mice. A mouse POF model was induced by subcutaneous injection of d-gal (200 mg/kg/day) daily for 42 days. Mice in the curcumin group received both d-gal treatment and intraperitoneal injection of curcumin (100 mg/kg/day) for 42 days. Ovarian function, oxidative stress and apoptosis were evaluated. The P, E2 and SOD levels were higher, and the FSH, LH and MDA levels were significantly lower in the curcumin group than those in the d-gal group. The proportion of primordial follicles was also significantly higher in the curcumin group than that in the d-gal group. In addition, curcumin treatment after d-gal administration resulted in significantly lower Sod2, Cat, 8-OhdG, 4-HNE, NTY and senescence-associated protein P16 expression levels, higher Amh expression levels and less apoptosis in granulosa cells than was observed in the d-gal group. Moreover, the p-Akt, Nrf2 and HO-1 protein expression levels were significantly higher and the apoptosis-related cleaved caspase-3 and -9 protein expression levels were markedly lower in the curcumin group than in the d-gal group. In conclusion, curcumin effectively inhibited d-gal-induced oxidative stress, apoptosis and ovarian injury via a mechanism involving the Nrf2/HO-1 and PI3K/Akt signaling pathways, suggesting that curcumin is a potential protective agent against POF.

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“…2010 ), anti-inflammatory ( Ueki et al . 2013 ), anti-apoptotic ( Geng et al . 2017 ) and antibacterial ( Mun et al .…”

Section: Discussionmentioning

confidence: 99%

Curcumin exerts a protective effect against premature ovarian failure in mice

Yan

Dai

et al. 2018

Journal of Molecular Endocrinology

123

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“…Experimental AKI induced by glycerol injection is the most commonly used experimental model of RM 1 , 11 , 12 and is characterized by intense cortical acute tubular necrosis and inflammatory cell infiltration 13 . Curcumin is an active component in turmeric rhizomes ( Curcuma Longa Linn ), and is a polyphenolic curcuminoid that accounts for 3–5% of turmeric 14 which has been shown to have antioxidant 15 – 18 , anti-inflammatory 19 – 21 , anti-apoptotic 22 and anti-bacterial 23 functions. The role of curcumin as a protective agent against renal injury induced by gentamicin, contrast agent, cisplatin and diabetes has been previously investigated 24 – 32 .…”

Section: Introductionmentioning

confidence: 99%

Effect of curcumin on glycerol-induced acute kidney injury in rats

Pan

et al. 2017

Sci Rep

106

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The aim of this study was to investigate the protective role and underlying mechanisms of curcumin on glycerol-induced acute kidney injury (AKI) in rats. Glycerol (10 ml/kg BW, 50% v/v in sterile saline, i.m.) was used to induce AKI, followed by curcumin (200 mg/kg/day, p.o.) administration for 3 days. To confirm renal damage and the effects of curcumin on AKI, serum BUN, Scr, and CK as well as renal SOD, MDA, GSH-Px were measured. Additionally, morphological changes were identified by H&E staining and transmission electron microscopy. The expression of several factors including chemotactic factor MCP-1, proinflammatory cytokines including TNF-α and IL-6, as well as the kidney injury markers, as Kim-1 and Lipocalin-2 were also assessed using q-PCR. Finally, cell apoptosis in renal tissue was detected using in situ TUNEL apoptosis fluorescence staining and expression of proteins associated with apoptotic, oxidative stress and lipid oxidative related signaling pathways were detected using immunohistochemical staining and western blot. The results showed that curcumin exerts renoprotective effects by inhibiting oxidative stress in rhabdomyolysis-induced AKI through regulation of the AMPK and Nrf2/HO-1 signaling pathways, and also ameliorated RM-associated renal injury and cell apoptosis by activating the PI3K/Akt pathway.

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“…A common complication of cisplatin administration is AKI [ 28 ]. PTEN acts as a tumor suppressor by negatively regulating the PI3K signaling pathway, which plays an important role in AKI [ 29 , 30 , 31 ], and studies have indicated that PTEN is involved in the mechanism of AKI [ 8 , 32 ]. However, the role of PTEN in cisplatin-induced AKI is unknown.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of PTEN activity aggravates cisplatin-induced acute kidney injury

et al. 2017

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Cisplatin (cis-Diamminedichloroplatinum II) has been widely and effectively used in chemotherapy against tumors. Nephrotoxicity due to cisplatin is one of the most common clinical causes of acute kidney injury (AKI), which has a poor prognosis and high mortality. The signaling mechanisms underlying cisplatin-induced AKI are not completely understood. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a tumor suppressor that negatively regulates the cell-survival pathway and is considered a double-edged sword in organ damage. In this study, we examined the effect that inhibiting PTEN activity in experimental models of cisplatin-induced AKI had on the degrees of AKI. Compared with vehicle mice, mice treated with bpV(pic) (specific inhibitor of PTEN) had exacerbated renal damage due to cisplatin-induced AKI. Furthermore, inhibition of PTEN activity increased cell apoptosis in the kidneys of mice induced by cisplatin. More inflammatory cytokines were activated after cisplatin treatment in mice of the bpV(pic)-treated group compared with vehicle mice, and these inflammatory cytokines may be partially derived from bone marrow cells. In addition, inhibiting PTEN activity decreased the phosphorylation of p53 in the pathogenesis of cisplatin-induced AKI. In summary, our study has demonstrated that inhibiting PTEN activity aggravates cisplatin-induced AKI via apoptosis, inflammatory reaction, and p53 signaling pathway. These results indicated that PTEN may serve as a novel therapeutic target for cisplatin-induced AKI.

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Biological Membrane-Packed Mesenchymal Stem Cells Treat Acute Kidney Disease by Ameliorating Mitochondrial-Related Apoptosis

Cited by 38 publications

References 29 publications

Curcumin exerts a protective effect against premature ovarian failure in mice

Curcumin exerts a protective effect against premature ovarian failure in mice

Effect of curcumin on glycerol-induced acute kidney injury in rats

Inhibition of PTEN activity aggravates cisplatin-induced acute kidney injury

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