Baicalin attenuates adriamycin-induced nephrotic syndrome by regulating fibrosis procession and inflammatory reaction

Tan Ning; Sun Chen-Xia; Zhu Hui-Jun; Li De-Yu; Huang Sheng-Guang; He Shou-Di

doi:10.1007/s13258-021-01107-x

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자료유형: 학술저널

저자정보: Tan Ning (Huazhong University of Science and Technology Union Shenzhen Hospital (Nanshan Hospital)) Sun Chen-Xia (Huazhong University of Science and Technology Union Shenzhen Hospital (Nanshan Hospital)) Zhu Hui-Jun (Huazhong University of Science and Technology Union Shenzhen Hospital (Nanshan Hospital)) Li De-Yu (Huazhong University of Science and Technology Union Shenzhen Hospital (Nanshan Hospital)) Huang Sheng-Guang (Huazhong University of Science and Technology Union Shenzhen Hospital (Nanshan Hospital)) He Shou-Di (Huazhong University of Science and Technology Union Shenzhen Hospital (Nanshan Hospital))

저널정보: 한국유전학회 Genes & Genomics Genes & Genomics Vol.43 No.9

발행연도: 2021.9

수록면: 1,011 - 1,021 (11page)

DOI: 10.1007/s13258-021-01107-x

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Background Baicalin has anti-infammatory, antibacterial, blood platelet aggregation-inhibiting, free oxygen radical-clearing, and endotoxin-decreasing properties. However, its molecular mechanism involved in the treatment of Adriamycin-induced nephrotic syndrome (NS) is still unclear. Objective This study aimed to explore the efects of baicalin on Adriamycin-induced nephrotic syndrome (NS) and to characterize the genes involved in this progression. Methods We established Adriamycin-induced NS model in 32 rats and used six rats in Sham group. Urinary total protein content and creatinine serum were assessed as physiological indicators. H&E staining was used to observe the pathological changes. We determined gene expression profles using transcriptome sequencing in the rat kidney tissues from Sham, Adriamycin, and Adriamycin+baicalin groups. KEGG was carried out to analyze the enriched pathways of diferentially expressed genes among these groups. Results Baicalin treatment relieved renal injury in NS rats. Expression of 363 genes was signifcantly diferent between the Adriamycin and Adriamycin+baicalin M groups. Most of the diferentially expressed genes were enriched in pathways involved in epithelial-mesenchymal transition (EMT), fbrosis, apoptosis, and infammation. Conclusions Overall, these data suggest that Adriamycin-induced NS can be attenuated by baicalin through the suppression of fbrosis-related genes and infammatory reactions. Baicalin is a potential drug candidate for the treatment of NS, and the identifed genes represent potential therapeutic targets.

#Nephrotic syndrome #Baicalin #Transcriptome sequencing #Fibrosis #Inflammatory reaction

참고문헌 (36)

참고문헌 신청

Adams JC / 2011 / The thrombospondins / Cold Spring Harb Perspect Biol 3:a009712

Bertani T / 1982 / Adriamycin-induced nephrotic syndrome in rats : sequence of pathologic events / Lab Investig 46:16~23

Bhattacharyya S / 2016 / Tenascin-C drives persistence of organ fbrosis / Nat Commun 7:11703

Carvajal G / 2008 / Angiotensin II activates the Smad pathway during epithelial mesenchymal transdiferentiation / Kidney Int 74:585~595

Chan SC / 2018 / Mechanism of fbrosis in HNF1Brelated autosomal dominant tubulointerstitial kidney disease / J Am Soc Nephrol 29:2493~2509

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