Objective In China, the occurrence rule, mechanisms and prevention measures of diseases under extreme weather are few reported and which (del) only focused (focus) on pathophysiological manifestation rather than molecular mechanism level. So (del) (Thus,) further study in this work will be carried out from molecular cytological level. This study explored (del) the effect of hyperthermia on ventricular cardiomyocytes and the participative roles of classic MAPK - ERK5 pathways on hyperthermia induced cardiomyocytes damage.
Methods Neonatal rat ventricular cardiac myocytes (NRVM) were isolated from the hearts of 1- to 3-day-old Sprague Dawley rats. NRVM were exposed to a hyperthermia (42°C, 60 min) environment. The degree of cell damage was observed at 0, 4, 8, 12, 16, and 24 h after recovery. The effects of hyperthermia on myocardial cells were probed by evaluating lactate dehydrogenase (LDH) release, cells beating rate and rhythm and viability (assessed by MTS assay). Apoptosis was detected using an annexin V-FITC/propidium iodide (PI) staining binding assay. Using western blot semi-quantitating Bim and extracellular signal-related kinase (ERK5) /phosphorylated extracellular signal-related kinase (p-ERK)(??). Using PD98059 as an inhibitor of MAPK pathways, semi-quantitating Bim by western blot(??).
Results 1. The beating rate of myocardial cells was slightly decreased immediately after temperature recovery, (del)(and) gradually decreased with time prolonged, and the (del)(.) Cell viability was (del) decreased (p<0.05);(and) the activity of lactate dehydrogenase was (del) increased (p<0.05). 2. Based on western blot analysis, the elevation of Bim protein expression occurred at recovery time (8 h) and (del)(,) peaked at 12 h(,) then went down slowly at 24 h after hyperthermia (p<0.05); ERK5 pathway responding to hyperthermia treatment (p<0.05). 3. Levels of Bim slightly decreased at (in) PD98059 group compared with hyperthermia group (p<0.05).
Conclusions Hyperthermia induces myocardial cells damage with apoptosis as main type. ERK5 participated the injure process of hyperthermia and Bim played its role via a MAPK-ERK5 pathway.