N-n-Butyl Haloperidol Iodide Ameliorates Cardiomyocytes Hypoxia/Reoxygenation Injury by Extracellular Calcium-Dependent and -Independent Mechanisms

Table 2

Effects of F₂, and ERK1/2 inhibitors and activator on LDH level, cTnI level, and cell viability in extracellular-calcium-free myocardial H/R (𝑛=9).

Group	LDH (U/mL)	cTnI (ng/mL)	Survival rate (%)
0CaCon	968.65 ± 12.37	0.17 ± 0.01	100.00
0CaH/R	1342.35 ± 15.82*	0.84 ± 0.03*	50.66 ± 1.90*
0CaH/R + F2	1135.16 ± 22.33^*#	0.62 ± 0.04^*#	67.38 ± 2.94^*#
0CaH/R + U0126	1155.04 ± 24.24^*#	0.69 ± 0.03^*#	62.81 ± 4.58^*#
0CaH/R + PD98059	1261.39 ± 14.20^*#	0.53±0.02^∗#†	57.73 ± 2.71^*#
0CaCon + EGF	1019.90±17.16^#†	0.17±0.01^#†	94.01±4.70^#†
0CaH/R + F2 + EGF	1421.43±17.16^∗†	0.77±0.05^∗†	53.17±2.48^∗†

F₂, N-n-butyl haloperidol iodide; LDH: lactate dehydrogenase; cTnI: cardiac troponin I; H/R: hypoxia/reoxygenation. *𝑃<0.05 versus 0CaCon group; ^#𝑃<0.05 versus 0CaH/R group; ^†𝑃<0.05 versus 0CaH/R + F₂ group.