Retracted: Resistin-Like Molecule Beta (RELM-β) Regulates Proliferation of Human Diabetic Nephropathy Mesangial Cells via Mitogen-Activated Protein Kinases (MAPK) Signaling Pathway

Wang, Yun-Qian; Fan, Congcong; Chen, Bao‐Ping; Shi, Jun

doi:10.12659/msm.936542

Cited by 2 publications

(2 citation statements)

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“…The MAPK signaling pathway regulates various inflammatory responses related to renal fibrosis. Intriguingly, it has been shown that inhibiting the MAPK pathway can attenuate DN [ 60 , 61 , 62 ]. On the other hand, the MAPK pathway is a classical pathway that can initiate the production of inflammatory mediators and NFκB activation indirectly or directly.…”

Section: Discussionmentioning

confidence: 99%

Diphenyl Diselenide Alleviates Tert-Butyl Hydrogen Peroxide-Induced Oxidative Stress and Lipopolysaccharide-Induced Inflammation in Rat Glomerular Mesangial Cells

Wang

Huan

Liu

et al. 2022

IJMS

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Hyperglycemia, oxidative stress, and inflammation play key roles in the onset and development of diabetic complications such as diabetic nephropathy (DN). Diphenyl diselenide (DPDS) is a stable and simple organic selenium compound with anti-hyperglycemic, anti-inflammatory, and anti-oxidative activities. Nevertheless, in vitro, the role and molecular mechanism of DPDS on DN remains unknown. Therefore, we investigated the effects of DPDS on tert-butyl hydrogen peroxide (t-BHP)-induced oxidative stress and lipopolysaccharide (LPS)-induced inflammation in rat glomerular mesangial (HBZY-1) cells and explored the underlying mechanisms. DPDS attenuated t-BHP-induced cytotoxicity, concurrent with decreased intracellular ROS and MDA contents and increased SOD activity and GSH content. Moreover, DPDS augmented the protein and mRNA expression of Nrf2, HO-1, NQO1, and GCLC in t-BHP-stimulated HBZY-1 cells. In addition, DPDS suppressed LPS-induced elevations of intracellular content and mRNA expression of interleukin (IL)-6, IL-1β and TNF-α. Furthermore, LPS-induced NFκB activation and high phosphorylation of JNK and ERK1/2 were markedly suppressed by DPDS in HBZY-1 cells. In summary, these data demonstrated that DPDS improves t-BHP-induced oxidative stress by activating the Nrf2/Keap1 pathway, and also improves LPS-induced inflammation via inhibition of the NFκB/MAPK pathways in HBZY-1 cells, suggesting that DPDS has the potential to be developed as a candidate for the prevention and treatment of DN.

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Section: Discussionmentioning

confidence: 99%

Diphenyl Diselenide Alleviates Tert-Butyl Hydrogen Peroxide-Induced Oxidative Stress and Lipopolysaccharide-Induced Inflammation in Rat Glomerular Mesangial Cells

Wang

Huan

Liu

et al. 2022

IJMS

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“…Mice subjected to a high-glucose diet for 30 days exhibit upregulated GLUT-2 expression and accumulated GLUT-2 transporters in the BBM [ 43 ]. The levels of GLUT-2 can be quantified in a mouse model of diabetes using the hyperinsulinemic-euglycemic clamp.…”

Section: The Links Between Glut-2 and Diabetes Pathogenesismentioning

confidence: 99%

Physiological functions of glucose transporter-2: From cell physiology to links with diabetes mellitus

Shen,

Hou,

Zhao

et al. 2024

Heliyon

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Retracted: Resistin-Like Molecule Beta (RELM-β) Regulates Proliferation of Human Diabetic Nephropathy Mesangial Cells via Mitogen-Activated Protein Kinases (MAPK) Signaling Pathway

Cited by 2 publications

References 1 publication

Diphenyl Diselenide Alleviates Tert-Butyl Hydrogen Peroxide-Induced Oxidative Stress and Lipopolysaccharide-Induced Inflammation in Rat Glomerular Mesangial Cells

Diphenyl Diselenide Alleviates Tert-Butyl Hydrogen Peroxide-Induced Oxidative Stress and Lipopolysaccharide-Induced Inflammation in Rat Glomerular Mesangial Cells

Physiological functions of glucose transporter-2: From cell physiology to links with diabetes mellitus

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