Polydatin-loaded chitosan nanoparticles ameliorates early diabetic nephropathy by attenuating oxidative stress and inflammatory responses in streptozotocin-induced diabetic rat

El-Hameed, Abeer Mohamed Abd

doi:10.1007/s40200-020-00699-7

Cited by 29 publications

(16 citation statements)

References 58 publications

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“…Polydatin (PD, C 20 H 22 O 8 ) is a natural active ingredient extracted from the dried roots of the perennial herb Polygonum cuspidatum Sieb. et Zucc., which might play a potential therapeutic role in various kidney disorders, such as AKI [7][8][9][10][11][12][13][14][15][16], diabetic nephropathy [17][18][19][20][21][22][23][24], lupus nephritis [25], and hyperuricemia [26][27][28], and has been used to treat patients with irritable bowel syndrome in Europe [29]; moreover, PD has been shown to exhibit mechanisms to antioxidant stress, anti-inflammation, and antifibrosis characteristics; improvement of mitochondrial damage; and regulation of autophagy [9,30,31]. Resveratrol, an aglycone of PD, has been verified to ameliorate myocardial and liver damage caused by iron overload [32][33][34]; moreover, it has been confirmed that resveratrol can reduce iron load in hemodialysis patients in clinical studies [35].…”

Section: Introductionmentioning

confidence: 99%

Polydatin Attenuates Cisplatin-Induced Acute Kidney Injury by Inhibiting Ferroptosis

Zhou

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Cisplatin is widely used in the treatment of solid tumors, but its application is greatly limited due to its nephrotoxicity; thus, there is still no effective medicine for the treatment of cisplatin-induced acute kidney injury (Cis-AKI). We previously identified that polydatin (PD) exerts nephroprotective effects by antioxidative stress in AKI models. Recent evidence suggests that oxidative stress-induced molecular events overlap with the process of ferroptosis and that there are common molecular targets, such as glutathione (GSH) depletion and lipid peroxidation. Nevertheless, whether the nephroprotective effect of PD is related to anti-ferroptosis remains unclear. In this study, the inhibitory effect of PD on ferroptosis was observed in both cisplatin-treated HK-2 cells (20 μM) in vitro and a Cis-AKI mouse model (20 mg/kg, intraperitoneally) in vivo, characterized by the reversion of excessive intracellular free iron accumulation and reactive oxygen species (ROS) generation, a decrease in malondialdehyde (MDA) content and GSH depletion, and an increase in glutathione peroxidase-4 (GPx4) activity. Remarkably, PD dose-dependently alleviated cell death induced by the system Xc− inhibitor erastin (10 μM), and the effect of the 40 μM dose of PD was more obvious than that of ferrostatin-1 (1 μM) and deferoxamine (DFO, 100 μM), classical ferroptosis inhibitors. Our results provide insight into nephroprotection with PD in Cis-AKI by inhibiting ferroptosis via maintenance of the system Xc−-GSH-GPx4 axis and iron metabolism.

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Section: Introductionmentioning

confidence: 99%

Polydatin Attenuates Cisplatin-Induced Acute Kidney Injury by Inhibiting Ferroptosis

Zhou

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…mTOR could improve the autophagy activity and reduce the apoptosis of chondrocytes in a KOA, further reduce the degree of OA [28]. It has been proved that polydatin regulated important molecules involved in autophagy and in ammation signaling pathways in bovine mammary epithelial cells [29], acute kidney injury [30,31] and myocardial injury in diabetic rats [32,33]. In this study, it was found that the effects of polydatin on autophagy induction was mTORdependent and regulated by AMPK.…”

Section: Abbreviationsmentioning

confidence: 82%

Polydatin Protects Against Articular Cartilage Degeneration by Regulating Autophagy Mediated by AMPK/Mtor Signaling Pathway

Yu³

et al. 2021

Preprint

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Background: Knee osteoarthritis (KOA) is one of the leading causes of disability, and its etiopathogenesis is not completely understood. Polydatin has the potential effect on the treatment of KOA, but the mechanism is not clear.Methods: After an KOA rat model was established by anterior cruciate ligament transection, KOA rats were treated with polydatin (4 mg/kg) for 30 days. Subsequently, cartilage tissues were collected from rats and detected by HE, TUNEL staining and Western blotting to evaluate the pathological damage, apoptosis and autophagy activity. Then, human chondrocyte C28/I2 cells were stimulated by LPS to induce a KOA model in vitro, and the effects of polydatin on the C28/I2 cell viability, apoptosis and autophagy were also detected. In addition, the mechanism of polydatin on KOA in C28/I2 cells was investigated, and the effect of an AMPK inhibitor (Dorsomorphin 2HCl) on the proliferation and apoptosis of polydatin administrated-cells were also detected. Results: After treated with polydatin, the pathological damage of rat cartilage tissues were ameliorated, cells apoptosis was inhibited and autophagy was activated in KOA rats. Meanwhile, polydatin also ameliorated the proliferation and apoptosis of C28/I2 cells, the expression of autophagy-related proteins, LC3II/LC3I, Beclin-1, and p-AMPK/AMPK were up-regulated, p-mTOR/mTOR was down-regulated by polydatin in C28/I2 cells. Interestingly, relative results showed that the improvement effect of polydatin on LPS-sdtimulated-C28/I2 cells was blocked by AMPK/mTOR inhibitor, Dorsomorphin 2HCl. Conclusion: Our research showed that polydatin reduces apoptosis and activate autophagy both in a rat model of KOA and C28/I2 cell model by AMPK/mTOR signaling pathway, which provides the basis for further investigations into the potential therapeutic impact of polydatin in KOA.

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“…Additionally, interestingly, resveratrol and ramipril co-treatment showed reversibility of glomerulosclerosis in early stage DN, supporting the efficiency of a combined therapeutic strategy in the early DN intervention [ 58 ]. Polydatin has been also shown to protect against renal dysfunction in DN by mechanisms including the attenuation of mitochondrial, reversion of apoptosis, suppression of oxidative stress, and mitigation of renal inflammation and fibrosis [ 59 , 60 , 61 , 62 , 63 , 64 ]. Punicalagin, the major hydrolysable tannin from pomegranate, whose metabolism involves the formation of gallic acid, has been also associated with DN protection.…”

Section: Implication Of Polyphenols In Renal Pathophysiologymentioning

confidence: 99%

Polyphenols and Their Metabolites in Renal Diseases: An Overview

Guerreiro

Ferreira-Pêgo

Carregosa

et al. 2022

Foods

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Kidney diseases constitute a worldwide public health problem, contributing to morbidity and mortality. The present study aimed to provide an overview of the published data regarding the potential beneficial effects of polyphenols on major kidney diseases, namely acute kidney injury, chronic kidney disease, diabetic nephropathy, renal cancer, and drug-induced nephrotoxicity. This study consists of a bibliographical review including in vitro and in vivo studies dealing with the effects of individual compounds. An analysis of the polyphenol metabolome in human urine was also conducted to estimate those compounds that are most likely to be responsible for the kidney protective effects of polyphenols. The biological effects of polyphenols can be highly attributed to the modulation of specific signaling cascades including those involved in oxidative stress responses, anti-inflammation processes, and apoptosis. There is increasing evidence that polyphenols afford great potential in renal disease protection. However, this evidence (especially when in vitro studies are involved) should be considered with caution before its clinical translation, particularly due to the unfavorable pharmacokinetics and extensive metabolization that polyphenols undergo in the human body. Future research should consider polyphenols and their metabolites that indeed reach kidney tissues.

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Polydatin-loaded chitosan nanoparticles ameliorates early diabetic nephropathy by attenuating oxidative stress and inflammatory responses in streptozotocin-induced diabetic rat

Cited by 29 publications

References 58 publications

Polydatin Attenuates Cisplatin-Induced Acute Kidney Injury by Inhibiting Ferroptosis

Polydatin Attenuates Cisplatin-Induced Acute Kidney Injury by Inhibiting Ferroptosis

Polydatin Protects Against Articular Cartilage Degeneration by Regulating Autophagy Mediated by AMPK/Mtor Signaling Pathway

Polyphenols and Their Metabolites in Renal Diseases: An Overview

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