Novel pectin-like polysaccharide from Panax notoginseng attenuates renal tubular cells fibrogenesis induced by TGF-β

Renal fibrosis is the final common result of a variety of progressive injuries leading to chronic renal failure. However, there are no effective clinical available drugs for the treatment. Notoginsenoside from Panax notoginseng could ameliorate renal fibrosis. We hypothesized that polysaccharide from this herb might have similar bioactivity. Here, we elucidated structure of a novel pectin-like polysaccharide designed SQD4S2 with a netty antenna backbone of glucogalacturonan substituted by glucoarabinan, glucurogalactan and galactose residues from this herb. Interestingly, SQD4S2 could reverse the morphological changes of human renal tubular HK-2 cells induced by TGF-beta. Mechanism study suggested that this bioactivity might associate with N-cadherin (CDH2), Snail (SNAI1), Slug (SNAI2) depression and E-cadherin (CDH1) enhancement. In addition, SQD452 could impede critical fibrogenesis associated molecules such as alpha-SMA, fibronectin, vimentin, COL1A1, COL3A1, FN1 and ACTA2 expression induced by TGF-beta in HK-2 cells. Current findings outline a novel leading polysaccharide for against renal fibrosis new drug development.

Automated summary

This study discovered that a polysaccharide named SQD4S2 extracted from Panax notoginseng could reverse the morphological changes of human renal tubular HK-2 cells induced by TGF-beta and impede critical fibrogenesis associated molecules expression, indicating the potential of SQD4S2 as a novel leading polysaccharide for new drug development against renal fibrosis.