【摘 要】
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Purpose: We sought to assess whether heat-induced autophagy, apoptosis and cell damage in H9c2 cells can be affected by pre-inducing HSP70 (heat shock protein 70).Materials and methods: Cell viability
【机 构】
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Department of Nursing, Shu-Zen Junior College of Medicine and Management, Kaohsiung City, Taiwan
【出 处】
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第九届海峡两岸心血管科学研讨会暨首届台湾南部国际心脑血管科学研讨会
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Purpose: We sought to assess whether heat-induced autophagy, apoptosis and cell damage in H9c2 cells can be affected by pre-inducing HSP70 (heat shock protein 70).Materials and methods: Cell viability was determined using 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyl tetrazolium bromide staining and a lactate dehydrogenase assay.Apoptosis was evidenced using both flow cytometry and counting caspase-3 positive cells, whereas autophagy was evidenced by the increased LC3-Ⅱ expression and lysosomal activity.Results: The viability of H9c2 cells was temperature-dependently (40-44 ℃) and timedependently (90-180 min) significantly (p<0.05) reduced by severe heat, which caused cell damage, apoptosis and autophagy.Heat-induced cell injury could be attenuated by pretreatment with 3-methylademine (an autophagy inhibitor) or Z-DEVD-FMK (a caspase-3 inhibitor).Neither apoptosis nor autophagy over the levels found in normothermic controls was induced in heat-shock preconditioned controls (no subsequent heat injury).The beneficial effects of mild heat preconditioning (preventing heat-induced cell damage, apoptosis and autophagy) were significantly attenuated by inhibiting HSP70 overexpression with triptolide (Tripterygium wilfordii) pretreatment.Conclusion: We conclude that pre-inducing HSP70 attenuates heat-stimulated cell autophagy, apoptosis and damage in the heart.However, this requires in vivo confirmation.
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