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Paeoniflorin Inhibits Tgf-Beta 1-Smad2/3 And Nf-Kappa B Signaling Pathways In High Fat Diet-Induced Kidney Injury And Inflammatory Responses

INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE(2018)

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摘要
Due to the high morbidity and mortality rates, kidney diseases have been treated as a global health problem. However, the causes of their formation and development remains to be fully elucidated. High fat diet (HFD)-induced kidney injury has attracted increasing attention. Paeoniflorin, an anti-inflammatory chemical compound found in the herbal medicine derived from Paeonia lactiflora Pall. Previous investigations of paeoniflorin have found it possesses several pharmacological effects, including anti-inflammatory, neuroprotective effects, and suppression of insulin resistance. Therefore, in this study, we will examine the underlying molecular mechanisms of paeoniflorin in the inhibition of HFD-induced kidney fibrosis. Rats fed with HFD were treated with or without paeoniflorin to investigate whether it offers a protective effect, and to determine the underlying molecular mechanism that could remit renal fibrosis. Reverse transcription-quantitative polymerase chain reaction, western blot analyses, Masson's staining and immunohistochemical analyses were performed to analyze the mRNA and protein expression of associated indicators in the treatment groups. The oral glucose and insulin tolerance, urinary protein and serum creatinine analyses were also performed to indicate changes in the metabolic and kidney functions of the rats. ELISA analysis was utilized to measure the effects of the inflammatory cytokines in the serum. The results indicated that paeoniflorin treatment suppressed renal fibrosis and the production of inflammatory cytokines by altering expression of NF-kappa B pathways and TGF-beta 1/Smad-in the kidneys from the HFD-fed rats. These findings provide a potential approach for treating fat rich diet-stimulated kidney-related diseases using natural products.
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关键词
Paeoniflorin, high fat diet, kidney fibrosis, TGF-beta 1, inflammation
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