ArticleRSC advances2018
Protective effects of SKLB023 on a mouse model of unilateral ureteral obstruction by the modulation of gut microbiota.
Article in RSC advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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8 authors at 1 institution in 4 countries.
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Abstract
Renal interstitial fibrosis is the common pathway underlying the progression of chronic kidney disease (CKD) to end-stage renal disease (ESRD) and the corresponding therapies are limited. Quantitative and qualitative alterations in gut microbiota are noted in patients with CKD and ESRD. In our previous study, SKLB023 exhibited antifibrotic effects by interfering TGF-β1/Smad3 signaling in obstructive nephropathy. However, it remained unclear that oral administration of SKLB023 drives the alteration of gut microbiota to attenuate renal fibrosis. In the study, the marked inflammation and interstitial fibrosis were found in the kidney tissues of unilateral ureteral obstruction (UUO) mice. While treatment with SKLB023 significantly alleviated renal interstitial fibrosis and reduced serum proinflammatory cytokines TNF-α, IL-6 levels. Importantly, SKLB023 derived the modulation of gut microbiota with the increasing similarity between the composition of gut microbiota in the control and UUO. The number of
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