Cocoa ameliorates renal injury in Zucker diabetic fatty rats by preventing oxidative stress, apoptosis and inactivation of autophagy

Álvarez-Cilleros, David; López-Oliva, María Elvira; Ramos, Sonia

doi:10.1039/c9fo01806a

Cited by 14 publications

(14 citation statements)

References 56 publications

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“…Autophagy is associated with the progression of numerous diseases, such as inflammation and cancer ( 44 – 46 ). Previous reports have indicated that activation of autophagy ameliorates the symptoms of DN ( 47 – 49 ), which was similar to the results of the present in vitro study; knockdown of PFKFB3 activated autophagy. Results from the present study also indicated that PFKFB3 siRNA may mediate the expression of LC3, p-mTOR, p-AMPKα and SIRT1 in podocytes.…”

Section: Discussionsupporting

confidence: 93%

Silencing of PFKFB3 protects podocytes against high glucose‑induced injury by inducing autophagy

et al. 2021

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Diabetic nephropathy (DN) is a diabetic complication that threatens the health of patients with diabetes. In addition, podocyte injury can lead to the occurrence of DN. The protein 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) may be associated with diabetes; however, the effects of PFKFB3 knockdown by small interfering (si)RNA on the growth of podocytes remains unknown. To investigate the mechanism by which PFKFB3 mediates podocyte injury, MPC5 mouse podocyte cells were treated with high-glucose (HG), and cell viability and apoptosis were examined by Cell Counting Kit-8 assay and flow cytometry, respectively. In addition, the expression of autophagy-related proteins were measured using western blot analysis and immunofluorescence staining. Cell migration was investigated using a Transwell assay and phalloidin staining was performed to observe the cytoskeleton. The results revealed that silencing of PFKFB3 significantly promoted MPC5 cell viability and inhibited apoptosis. In addition, the migration of the MPC5 cells was notably downregulated by siPFKFB3. Moreover, PFKFB3 silencing notably reversed the HG-induced decrease in oxygen consumption rate, and the HG-induced increase in extracellular acidification rate was rescued by PFKFB3 siRNA. Furthermore, silencing of PFKFB3 induced autophagy in HG-treated podocytes through inactivating phosphorylated (p-)mTOR, p-AMPKα, LC3 and sirtuin 1, and activating p62. In conclusion, silencing of PFKFB3 may protect podocytes from HG-induced injury by inducing autophagy. Therefore, PFKFB3 may serve as a potential target for treatment of DN.

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Section: Discussionsupporting

confidence: 93%

Silencing of PFKFB3 protects podocytes against high glucose‑induced injury by inducing autophagy

et al. 2021

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“…10,16,18,19,22 Additionally, it has been shown that cocoa and EC can prevent or delay the injury associated with diabetes by reducing glycaemia and modulating oxidative stress. 16,18,19,22 After the consumption of flavanol-rich food, mono-and di-hydroxylated phenylpropionic, phenylacetic and hydroxybenzoic acids and conjugated forms are the most abundant metabolites in urine and plasma. 11 However, it has been proved that conjugation could be a reversible process in vivo, and as a result pure compounds could be accumulated in tissues.…”

Section: Discussionmentioning

confidence: 99%

“…Intracellular ROS were quantified by the DCFH assay as described elsewhere. 16,22 Briefly, the cells were cultured in 24-well plates (2 × 10 5 cells per well) and incubated with the different treatments. Then, 5 μM DCFH probe was added to the wells and kept for 30 min at 37°C.…”

Section: Reactive Oxygen Species (Ros) Generation Analysesmentioning

confidence: 99%

(−)-Epicatechin and the colonic metabolite 2,3-dihydroxybenzoic acid protect against high glucose and lipopolysaccharide-induced inflammation in renal proximal tubular cells through NOX-4/p38 signalling

2020

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“…Furthermore, to get further insights into the mechanisms for the protective effect of RLE intake during diabetes in kidney, we have also analyzed the involvement of apoptosis because it is well-demonstrated that oxidative stress can contribute to the regulation of this cell death event [51]. We found that the increase in NOX4 levels was associated with a significant growth of BAX/BCL-2 ratio in ZDF animals and this increase was completely prevented in ZDF rats treated with RLE (Figures 2 and 5).…”

Section: Discussionmentioning

confidence: 99%

Effects of a Red Orange and Lemon Extract in Obese Diabetic Zucker Rats: Role of Nicotinamide Adenine Dinucleotide Phosphate Oxidase

Damiano

Lauritano

Longobardi

et al. 2020

JCM

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Diabetic nephropathy (DN) is the primary cause of end-stage renal disease, worldwide, and oxidative stress has been recognized as a key factor in the pathogenesis and progression of DN. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase has the most important contribution to reactive oxygen species generation during the development of DN. Bioactive compound use has emerged as a potential approach to reduce chronic renal failure. Therefore, a red orange and lemon extract (RLE) rich in anthocyanins was chosen in our study, to reduce the toxic renal effects during the development of DN in Zucker diabetic fatty rat (ZDF). RLE effects were examined daily for 24 weeks, through gavage, in ZDF rats treated with RLE (90 mg/kg). At the end of the experiment, ZDF rats treated with RLE showed a reduction of the diabetes-associated up-regulation of both NOX4 and the p47-phox and p22-phox subunits, and restored the BAX/BCL-2 ratio respect to ZDF rats. Furthermore, RLE was able to reduce the oxidative DNA damage measured in urine samples in ZDF rats. This study showed that RLE could prevent the renal damage induced by DN through its capacity to inhibit NOX4 and apoptosis mechanisms.

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Cocoa ameliorates renal injury in Zucker diabetic fatty rats by preventing oxidative stress, apoptosis and inactivation of autophagy

Abstract: Cocoa prevents main processes involved in the development of diabetic nephropathy including redox imbalance, apoptosis and inhibition of autophagy.

Cited by 14 publications

References 56 publications

Silencing of PFKFB3 protects podocytes against high glucose‑induced injury by inducing autophagy

Silencing of PFKFB3 protects podocytes against high glucose‑induced injury by inducing autophagy

(−)-Epicatechin and the colonic metabolite 2,3-dihydroxybenzoic acid protect against high glucose and lipopolysaccharide-induced inflammation in renal proximal tubular cells through NOX-4/p38 signalling

Effects of a Red Orange and Lemon Extract in Obese Diabetic Zucker Rats: Role of Nicotinamide Adenine Dinucleotide Phosphate Oxidase

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