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Antioxidants attenuate high glucose-induced hypertrophic growth in renal tubular epithelial cells
Jau-Shyang Huang1, Lea-Yea Chuang, Jinn-Yuh Guh
1Department of Biological Science and Technology, Chung Hwa University of Medical Technology, Tainan, Taiwan, ROC. jaushyang12@hotmail.com
Abstract:
Hyperglycemia-induced oxidative stress is a key mediator of renal tubular hypertrophy in diabetic nephropathy (DN). The molecular mechanisms of antioxidants responsible for inhibition of renal tubular hypertrophy in DN are incompletely characterized. We now aim at verifying the effects of N-acetylcysteine (NAC) and taurine on cellular hypertrophy in renal tubular epithelial cells under high ambient glucose. We found that NAC and taurine treatments significantly attenuated high glucose (HG)-inhibited cellular growth and HG-induced hypertrophy. HG-induced Raf-1, p42/p44 mitogen-activated protein kinase (MAPK), Janus kinase 2 (JAK2), and signal transducer and activator of transcription 1 (STAT1) and STAT3 (but not STAT5) activation was markedly blocked by NAC and taurine. Moreover, NAC and taurine increased cyclin D1/cdk4 activation and suppressed p21(Waf1/Cip1) and p27(Kip1) expression in HG-treated cells. It seems that apoptosis was not observed in these treatments. There were no changes in bcl-2 and poly(ADP-ribose) polymerase expression, and mitochondrial cytochrome c release. However, NAC or taurine markedly inhibited the stimulation by HG of fibronectin and type IV collagen protein levels. It is concluded that both NAC and taurine significantly attenuated HG-induced activation of the Raf-1/MAPK and the JAK2-STAT1/STAT3 signaling pathways and hypertrophic growth in renal tubular epithelial cells.
Insights
N-acetylcysteine (NAC) and taurine combat high glucose-induced kidney cell growth and hypertrophy in diabetic nephropathy. These antioxidants inhibit key signaling pathways and reduce fibronectin and collagen levels.
Area of Science:
- Cell Biology
- Molecular Biology
- Nephrology
Background:
- Diabetic nephropathy (DN) involves hyperglycemia-driven oxidative stress, leading to renal tubular hypertrophy.
- The precise mechanisms by which antioxidants inhibit hypertrophy in DN are not fully understood.
Purpose of the Study:
- To investigate the effects of N-acetylcysteine (NAC) and taurine on renal tubular epithelial cells experiencing high glucose.
- To elucidate the molecular pathways targeted by NAC and taurine in mitigating hypertrophy.
Main Methods:
- Cultured renal tubular epithelial cells were exposed to high glucose conditions.
- The impact of NAC and taurine on cellular growth, hypertrophy, signaling pathways (Raf-1/MAPK, JAK2/STAT), cell cycle regulators, and extracellular matrix proteins was assessed.
Main Results:
- NAC and taurine significantly reduced high glucose-induced cellular hypertrophy and inhibited the activation of Raf-1/MAPK and JAK2-STAT1/STAT3 signaling pathways.
- These antioxidants modulated cell cycle proteins, increasing cyclin D1/cdk4 and decreasing p21/p27 expression.
- NAC and taurine suppressed high glucose-stimulated fibronectin and type IV collagen production without inducing apoptosis.
Conclusions:
- NAC and taurine effectively attenuate high glucose-induced hypertrophic growth in renal tubular epithelial cells.
- Their protective effects involve the inhibition of specific signaling cascades and extracellular matrix deposition, offering potential therapeutic strategies for diabetic nephropathy.
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