Wang, Fujing; Fan, Jiaer; Pei, Tingting; He, Zhuoen; Zhang, Jiaxing; Ju, Liliang; Han, Zhongxiao; Wang, Mingqing; Xiao, Wei published the artcile< Effects of shenkang pills on early-stage diabetic nephropathy in db/db mice via inhibiting AURKB/ RacGAP1/RhoA signaling pathway>, Product Details of C19H34O2, the main research area is shenkang nephroprotective agent AURKB RacGAP1 RhoA diabetic nephropathy; AURKB; LC/MS; RacGAP1; RhoA; diabetic nephropathy; shenkang pills; transcriptome.
Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, so there is an urgent need to suppress its development at early stage. Shenkang pills (SKP) are a hospital prescription selected and optimized from effective traditional Chinese medicinal formulas for clin. treatment of DN. In the present study, liquid chromatog.-quadrupole-time of flight-mass spectrometry (LC-Q-TOF-MS) and total contents qualification were applied to generate a quality control standard of SKP. For verifying the therapeutic effects of SKP, db/db mice were administered intragastrically with SKP at a human-equivalent dose (1.82 g/kg) for 4 wk. Moreover, the underlying mechanism of SKP were analyzed by the renal RNA sequencing and network pharmacol. LC-Q-TOF-MS identified 46 compounds in SKP. The total polysaccharide and organic acid content in SKP were 4.60 and 0.11 mg/mL, resp., while the total flavonoid, saponin, and protein content were 0.25, 0.31, and 0.42 mg/mL, resp. Treatment of SKP significantly reduced fasting blood glucose, improved renal function, and ameliorated glomerulosclerosis and focal foot processes effacement in db/db mice. In addition, SKP protected podocytes from injury by increasing nephrin and podocin expression. Furthermore, transcriptome analyses revealed that 430 and 288 genes were up and down-regulated in mice treated with SKP, relative to untreated controls. Gene ontol. enrichment anal. revealed that the differentially expressed genes mainly involved in modulation of cell division and chromosome segregation. Weighted gene co-expression network anal. and network pharmacol. anal. indicated that aurora kinase B (AURKB), Rac GTPase activating protein 1 (RacGAP1) and SHC binding, and spindle associated 1 (shcbp1) might be the core targets of SKP. This protein and Ras homolog family member A (RhoA) were found overexpression in db/db mice, but significantly decreased with SKP treatment. We conclude that SKP can effectively treat early-stage DN and improve renal podocyte dysfunction. The mechanism may involve down-regulation of the AURKB/RacGAP1/ RhoA pathway.
Frontiers in Pharmacology published new progress about Adenosine A1 receptors Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 112-63-0 belongs to class esters-buliding-blocks, and the molecular formula is C19H34O2, Product Details of C19H34O2.
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