Lobetyolin, a Q-marker isolated from Radix Platycodi, exerts protective effects on cisplatin-induced cytotoxicity in HEK293 cells

This study investigated the protective effect of lobetyolin (LBT), a Q-marker isolated from the roots of Platycodon grandiflorum (Radix Platycodi), against cisplatin-induced cytotoxicity in human embryonic kidney (HEK293) cells. Results showed that LBT at 20 & mu;M significantly prevented cisplatin-induced cytotoxicity by improving the viability of HEK293 cells, decreasing levels of MDA, and decreasing GSH content triggered by cisplatin. It also suppressed reactive oxygen species (ROS) levels. Molecular docking analysis revealed a strong binding affinity between LBT and the NF-& kappa;B protein, with a docking fraction of - 6.5 kcal/mol. These results provide compelling evidence suggesting a potential link between the visualization analysis of LBT and its protective mechanism, specifically implicating the NF-& kappa;B signaling pathway. LBT also reduced the expression level of tumor necrosis factor-alpha (TNF-& alpha;), phosphorylation NF-& kappa;B and I & kappa;B & alpha; in HEK293 cells which were increased by cisplatin exposure, leading to inhibition of inflammation. Furthermore, western blotting showed that LBT antagonized the up-regulation of Bax, cleaved caspase 3, 8, and 9 expression and inhibited the MAPK signaling pathway by down-regulating phosphorylation JNK, ERK, and p38, partially ameliorating cisplatin-induced cytotoxicity in HEK293 cells. Therefore, these results indicate that LBT has potentially protected renal function by inhibiting inflammation and apoptosis.

Automated summary

This study investigated the protective effect of lobetyolin (LBT) against cisplatin-induced cytotoxicity in HEK293 cells. Results showed that LBT improved the viability of HEK293 cells, decreased MDA levels, decreased GSH content, and suppressed ROS levels caused by cisplatin. Molecular docking analysis revealed a strong binding affinity between LBT and the NF-κB protein. LBT also inhibited inflammation and apoptosis in HEK293 cells.