Tranilast prevents renal interstitial fibrosis by blocking mast cell infiltration in a rat model of diabetic kidney disease was written by Yin, Dan-Dan;Luo, Jun-Hui;Zhao, Zhu-Ye;Liao, Ying-Jun;Li, Ying. And the article was included in Molecular Medicine Reports in 2018.Formula: C18H17NO5 This article mentions the following:
Renal interstitial fibrosis is a final pathway that is observed in various types of kidney diseases, including diabetic kidney disease (DKD). The present study investigated the effect of tranilast on renal interstitial fibrosis and the association between its role and mast cell infiltration in a rat model of DKD. A total of 30 healthy 6-wk-old male Sprague-Dawley rats were randomly divided into the following four groups: Normal control group; DKD model group; low-dose tranilast group (200 mg/kg/day); and high-dose tranilast group (400 mg/kg/day). The morphol. alterations of tubulointerstitial fibrosis were evaluated by Masson’s trichrome staining, while mast cell infiltration into the renal tubular interstitium was measured by toluidine blue staining and complement C3a receptor 1 (C3aR) immunohistochem. staining (IHC). The expression of fibronectin (FN), collagen I (Col-I), stem cell factor (SCF) and proto-oncogene c-kit (c-kit) was detected by IHC, western blotting and reverse transcription-quant.-polymerase chain reaction. The results demonstrated that tubulointerstitial fibrosis and mast cell infiltration were observed in DKD model rats, and this was improved dose-dependently in the tranilast treatment groups. The expression of FN, Col-I, SCF and c-kit mRNA and protein was upregulated in the tubulointerstitium of DKD model rats compared with the normal control rats, and tranilast inhibited the upregulated expression of these markers. Furthermore, the degree of SCF and c-kit expression demonstrated a significant pos. correlation with C3aR-pos. mast cells and the markers of renal interstitial fibrosis. The results of the present study indicate that mast cell infiltration may promote renal interstitial fibrosis via the SCF/c-kit signaling pathway. Tranilast may prevent renal interstitial fibrosis through inhibition of mast cell infiltration mediated through the SCF/c-kit signaling pathway. In the experiment, the researchers used many compounds, for example, 2-(3-(3,4-Dimethoxyphenyl)acrylamido)benzoic acid (cas: 53902-12-8Formula: C18H17NO5).
2-(3-(3,4-Dimethoxyphenyl)acrylamido)benzoic acid (cas: 53902-12-8) belongs to amides. Amides are pervasive in nature and technology. Proteins and important plastics like Nylons, Aramid, Twaron, and Kevlar are polymers whose units are connected by amide groups (polyamides); these linkages are easily formed, confer structural rigidity, and resist hydrolysis. Amides can be recrystallised from large quantities of water, ethanol, ethanol/ether, aqueous ethanol, chloroform/toluene, chloroform or acetic acid. The likely impurities are the parent acids or the alkyl esters from which they have been made. The former can be removed by thorough washing with aqueous ammonia followed by recrystallisation, whereas elimination of the latter is by trituration or recrystallisation from an organic solvent.Formula: C18H17NO5
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Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics