Extracellular superoxide dismutase ameliorates streptozotocin-induced rat diabetic nephropathy via inhibiting the ROS/ERK1/2 signaling

Kuo, Chia Wen; Shen, Chi–Yen; Tung, Yu Tang; Chen, Hsiao Ling; Chen, Yu-Hsuan; Chang, Wei-Feng; Cheng, Kai‐Chun; Yang, Su–Hua; Chen, Chuan-Mu

doi:10.1016/j.lfs.2015.04.018

Cited by 55 publications

(42 citation statements)

References 51 publications

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“…TGF-ß plays an important role in the diabetic glomerular pathology and is activated under high-glucose conditions [6]. In this study, the TGF-ß expression was assessed using IHC staining and western blot.…”

Section: Resultsmentioning

confidence: 99%

“…Hyperglycemia-induced excess superoxide, resulted from the formation of ROS, has been founded during DN in many studies [6, 24]. ROS levels are regulated by endogenous antioxidants and antioxidases including GSH and SOD, which indirectly reflects the body’s ability to clear ROS.…”

Section: Discussionmentioning

confidence: 99%

“…TGF-ß induces renal damage by activating its downstream signaling pathway, in which MAPK are included [6]. MAPK is an important intracellular signal transduction molecule, and it possesses multiple functions in regulating cellular growth, proliferation, differentiation and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…Enhanced oxidative stress and the activation of transforming growth factor-ß (TGF-ß) signaling pathway are the main molecular pathways mediated during DN [6]. The balance between antioxidant defense system, including dicarboxylic aldehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, upstream of the reactive oxygen species (ROS), determine the degree of oxidative stress [7, 8].…”

Section: Introductionmentioning

confidence: 99%

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Huangqi Decoction Ameliorates Streptozotocin-Induced Rat Diabetic Nephropathy through Antioxidant and Regulation of the TGF-β/MAPK/PPAR-γ Signaling

Han

Wang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Huangqi Decoction (HQD) has been traditionally used to treat diabetes mellitus in China. The present study was carried out to assess the protective effect of HQD on diabetic nephropathy (DN) using the streptozotocin-induced (STZ) diabetic rats. Methods: Diabetes was induced by a single intraperitoneal injection of STZ (60 mg/kg) in male Wistar rats. 40 diabetic rats were divided into 5 groups: vehicle-treated (DN group), 0.45, 0.15, 0.05 g/kg HQD-treated diabetic group (HQD group) and 1 mg/kg rosiglitazone-treated diabetic group (RGZ group). 16 normal rats were randomly divided into 2 groups: vehicle-treated normal control group (NC) and 0.45 g/kg HQD-treated normal control group (NC+0.45 g/kg HQD). At the end of 8-week experiment, we measured changes of renal pathological morphology, function, antioxidant enzyme levels and the activation of TGF-β/PPAR-γ/MAPK signaling pathway. Results: After HQD treatment, renal function, including blood urea nitrogen (BUN), 24-h albuminuria and blood glucose level were improved significantly; meanwhile, impaired kidney redox balance was diminished in diabetic rats. The activation of TGF-β, phospho-JNK, phospho-p44/42, p47 and p42 phox was blocked and the decrease in PPAR-γ in diabetic rats was attenuated by treatment with HQD in a dose-dependent manner. Conclusion: These results suggest that HQD shows therapeutic efficacy in DN characterized by renal dysfunction and pathological changes through hypoglycemic and antioxidant effects.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Huangqi Decoction Ameliorates Streptozotocin-Induced Rat Diabetic Nephropathy through Antioxidant and Regulation of the TGF-β/MAPK/PPAR-γ Signaling

Han

Wang

et al. 2017

Cell Physiol Biochem

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“…STZ not only reduces insulin receptor signaling and downstream proteins, including IRS‐1, IRS‐2, AMPK, and GLUT [26], but also influences glycolysis proteins, including GCK and PPAR‐γ [27–29], by activating the MAPKs pathway [29,30]. STZ increases reactive oxygen species (ROS), nitric oxide production, oxidative stress and mitochondrial dysfunction [30,31] to induce damage to pancreas beta cells [32], while the MAPKs pathway can be stimulated by ROS and oxidative stress [30–32]. Many studies have shown that DM, including the STZ‐induced DM model, is related to MAPKs pathway activation [29–32].…”

Section: Discussionmentioning

confidence: 99%

Eugenosedin‐A improves glucose metabolism and inhibits MAPKs expression in streptozotocin/nicotinamide‐induced diabetic rats

Shen

Lin

Yen

et al. 2017

The Kaohsiung J of Med Scie

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This study examined the effects of eugenosedin-A (Eu-A) in a streptozotocin (STZ)/nicotinamide-induced rat model of type II diabetes mellitus (T2DM). Six-week-old Sprague-Dawley rats were randomly divided into three groups: (1) RD group, normal rats fed a regular diet (RD), (2) DM group, T2DM rats fed a high-fat diet, and (3) Eu-A group, T2DM rats fed a high fat diet plus oral Eu-A (5 mg/kg/day). After 30 days, the DM group had higher body weight, higher blood glucose and lower insulin levels than the RD group. The DM group also had increased protein expression of glycogen synthase kinase (GSK) in liver and skeletal muscle and decreased protein expression of insulin receptor (IR), insulin receptor substrate-1 (IRS-1), IRS-2, AMP-activated protein kinase (AMPK), glucose transporter-4 (GLUT-4), glucokinase (GCK), and peroxisome proliferator-activated receptor γ (PPAR-γ). STZ/nicotinamide-induced T2DM increased the expression of mitogen-activated protein kinases (MAPKs: p38, ERK, JNK) and inflammatory p65 protein. In the Eu-A treated T2DM rats, however, blood glucose was attenuated and the insulin concentration stimulated. Changes in IR, IRS-1 and IRS-2 proteins as well as AMPK, GLUT-4, GCK, GSK, PPAR-γ, MAPKs, and inflammatory p65 proteins were ameliorated. These results suggested that Eu-A alleviates STZ/nicotinamide-induced hyperglycemia by improving insulin levels and glucose metabolism, and inhibiting the MAPKs- and p65-mediated inflammatory pathway.

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Anti-oxidative effects of superoxide dismutase 3 on inflammatory diseases

2019

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Extracellular superoxide dismutase ameliorates streptozotocin-induced rat diabetic nephropathy via inhibiting the ROS/ERK1/2 signaling

Cited by 55 publications

References 51 publications

Huangqi Decoction Ameliorates Streptozotocin-Induced Rat Diabetic Nephropathy through Antioxidant and Regulation of the TGF-β/MAPK/PPAR-γ Signaling

Huangqi Decoction Ameliorates Streptozotocin-Induced Rat Diabetic Nephropathy through Antioxidant and Regulation of the TGF-β/MAPK/PPAR-γ Signaling

Eugenosedin‐A improves glucose metabolism and inhibits MAPKs expression in streptozotocin/nicotinamide‐induced diabetic rats

Anti-oxidative effects of superoxide dismutase 3 on inflammatory diseases

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