Carnosine inhibits high glucose-induced mesangial cell proliferation through mediating cell cycle progression

Jia, Hui‐Zhen; Qi, Xiaodan; Fang, Shaohong; Jin, Yuhong; Han, Xiaoying; Wang, Yi; Wang, Aiming; Zhou, Hongyu

doi:10.1016/j.regpep.2008.12.004

Cited by 44 publications

(24 citation statements)

References 41 publications

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“…Scavenging of radicals by carnosine may, therefore, reduce ERK signalling in tumour cells followed by impaired survival and proliferation. Evidence supporting the idea of carnosine compromises signalling has been obtained (Jia et al 2009); carnosine was shown to inhibit mesangial cell proliferation in response to high glucose levels, the cell-cycle being arrested at the transition from G1 to S phase, which was accompanied by decreased phosphorylation of ERK 1/2 and p38 MAP kinase. Evidence that carnosine inhibits phosphorylation of ERK 1/2 and p38 MAP kinase was also obtained by Son et al (2008) using intestinal epithelial cells.…”

Section: Possible Mechanismsmentioning

confidence: 87%

Carnosine and cancer: a perspective

Gaunitz

Hipkiss

2012

Amino Acids

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The application of carnosine in medicine has been discussed since several years, but many claims of therapeutic effects have not been substantiated by rigorous experimental examination. In the present perspective, a possible use of carnosine as an anti-neoplastic therapeutic, especially for the treatment of malignant brain tumours such as glioblastoma is discussed. Possible mechanisms by which carnosine may perform its anti-tumourigenic effects are outlined and its expected bioavailability and possible negative and positive side effects are considered. Finally, alternative strategies are examined such as treatment with other dipeptides or b-alanine.

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Section: Possible Mechanismsmentioning

confidence: 87%

Carnosine and cancer: a perspective

Gaunitz

Hipkiss

2012

Amino Acids

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“…Previous studies have demonstrated that hyperglycaemia plays an important role in the pathogenesis of DN (Larkins and Dunlop, 1992; Feldt-Rasmussen, 2000). HG can promote the proliferation in glomerular mesangial cells (Jia et al, 2009). We also found that HG induced proliferation of HBZY-1 cells, and astilbin attenuated the induction.…”

Section: Discussionmentioning

confidence: 99%

Astilbin Inhibits High Glucose-Induced Inflammation and Extracellular Matrix Accumulation by Suppressing the TLR4/MyD88/NF-κB Pathway in Rat Glomerular Mesangial Cells

et al. 2018

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Diabetic nephropathy (DN) is characterized by inflammatory responses and extracellular matrix (ECM) accumulation. Astilbin is an active natural compound and possesses anti-inflammatory activity. The aim of this study was to evaluate the anti-inflammatory effect of astilbin on high glucose (HG)-induced glomerular mesangial cells and the potential mechanisms. The results showed that HG induced cell proliferation of HBZY-1 cells in a time-dependent manner, and astilbin inhibited HG-induced cell proliferation. The expression and secretion of inflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α), and ECM components, including collagen IV (Col IV) and fibronectin (FN), were induced by HG. Moreover, TGF-β1 and CTGF were also induced by HG. The induction by HG on inflammatory response and ECM accumulation was inhibited after astilbin treatment. Astilbin treatment also attenuated HG-induced decrease in expression of matrix metalloproteinase (MMP)-2 and MMP-9. The TLR4/MyD88/NF-κB pathway was activated by HG, and the inhibitor of TLR4 exhibited the same effect to astilbin on reversing the induction of HG. TLR4 overexpression attenuated the effect of astilbin on HG-induced inflammatory cytokine production and ECM accumulation. The results suggested that astilbin attenuated inflammation and ECM accumulation in HG-induced rat glomerular mesangial cells via inhibiting the TLR4/MyD88/NF-κB pathway. This work provided evidence that astilbin can be considered as a potential candidate for DN therapy.

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“…Furthermore, the data indicate that the substrate of CN-1, carnosine might be beneficial in relation to diabetic complications. Experimentally, it has been demonstrated that carnosine reduces lipid oxidation in kidneys and inhibits glucose-induced proliferation of mesangial cell [15,16]. Furthermore, accumulation of extracellular matrix and upregulation of profibrotic TGF-is preventable by carnosine in cultured human podocytes and mesangial cells, suggesting that carnosine is a protective factor in diabetic nephropathy [14].…”

Section: Introductionmentioning

confidence: 99%

Oral Carnosine Supplementation Prevents Vascular Damage in Experimental Diabetic Retinopathy

Pfister

Riedl

Wang

et al. 2011

Cell Physiol Biochem

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Backgrounds/Aims: Pericyte loss, vasoregression and neuroglial activation are characteristic changes in incipient diabetic retinopathy. In this study, the effect of the antioxidant and antiglycating dipeptide carnosine was studied on the development of experimental diabetic retinopathy. Materials/Methods: STZ-induced diabetic Wistar rats were orally treated with carnosine (1g/kg body weight/day). Retinal vascular damage was assessed by quantitative morphometry. Retinal protein extracts were analyzed for markers of oxidative stress, AGE-formation, activation of the hexosamine pathway and changes in the expression of Ang-2, VEGF and heat shock proteins Hsp27 and HO-1. Glial cell activation was analyzed using Western blot analysis and immunofluorescence of GFAP expression and retinal neuronal damage was histologically examined. Results: Oral carnosine treatment prevented retinal vascular damage after 6 months of experimental hyperglycemia. The protection was not caused by ROS- or AGE-inhibition, but associated with a significant induction of Hsp27 in activated glial cells and normalization of increased Ang-2 levels in diabetic retinas. A significant reduction of photoreceptors in retinas of carnosine treated animals was noted. Conclusion: Oral carnosine treatment protects retinal capillary cells in experimental diabetic retinopathy, independent of its biochemical function. The vasoprotective effect of carnosine might be mediated by the induction of protective Hsp27 in activated glial cells and normalization of hyperglycemia-induced Ang-2.

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Carnosine inhibits high glucose-induced mesangial cell proliferation through mediating cell cycle progression

Cited by 44 publications

References 41 publications

Carnosine and cancer: a perspective

Carnosine and cancer: a perspective

Astilbin Inhibits High Glucose-Induced Inflammation and Extracellular Matrix Accumulation by Suppressing the TLR4/MyD88/NF-κB Pathway in Rat Glomerular Mesangial Cells

Oral Carnosine Supplementation Prevents Vascular Damage in Experimental Diabetic Retinopathy

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