Abstract

BackgroundBrassica rapa L. (turnip) is an ancient plant grown on the Tibetan Plateau, which possesses functions of heat-clearing and toxin, enhancing oxygen. The primary objective of this study is to assess the potential protective effect of petroleum ether extract of turnip (PET) against ischemia and hypoxia. Basic proceduresTotal extract of turnip (TET) was extracted 3 times with petroleum ether at a ratio of 1:1 and the PET was concentrated and identified by UHPLC-MS. Pharmacological and drug-like properties prediction of major compounds of PET were determined by the SwissADME tool. The protein–protein interaction test for PET-Cerebral Ischemic Stroke-Oxidative Damage (PET-CIS-OD) common targets were calculated by the SRTING giant database. The molecular function, biological process and cell composition of core targets were analyzed by ClueGo and CluePedia. KEGG pathway analysis were used for calculating the potential pathway affected by the PET-CIS-OD common targets. Molecular docking were measured by AutoDockTools 1.5.7 and PyMol. Oxygen-Glucose Deprivation/Reperfusion (OGD/R) model were established for evaluating the changes of the OD markers. Western blotting was used to verify the core proteins in signaling pathways obtained by network pharmacology. Main findingsPET intervention increased antioxidant ability in HT22 cells. Furthermore, PET could effectively recovered the COXIV expression, inhibit the Bax levels (p < 0.01), strengthen the Bcl-2 levels (p < 0.05) in HT22 cells after OGD/R injury. Our calculation results and experimental results indicated that PET may act as a key intervention in CIS by enhancing the level of phospho-PI3K (p < 0.001), phospho-Akt (p < 0.01) and phospho-mTOR (p < 0.01) and lessening the levle of phospho-P38 (p < 0.01) and HIF-1α (p < 0.05). ConclusionsOur study systematically explored the potential function and regulatory mechanism of PET in CIS for the first time. The results indicated that PET may play neuroprotective effect against CIS by regulating PI3K/Akt/mTOR signaling pathway and MAPK signaling pathway, and exerting antioxidant and anti-apoptotic effects on OGD/R injury.

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