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. Author manuscript; available in PMC: 2017 Jun 1.
Published in final edited form as: J Recept Signal Transduct Res. 2015 Sep 29;36(3):261–270. doi: 10.3109/10799893.2015.1091475

Figure 2. α1-AR stimulation reduced lactate dehydrogenase release (A) or annexin V+ apoptosis (B) in WT neonatal myocytes undergoing glucose deprivation through a PKC-mediated pathway.

Figure 2

Figure 2

Neonatal myocytes seeded onto 96-well plates were subjected to normoxic conditions (control) or with low glucose concentrations (Glu−; 1.375mM) with or without α1-AR stimulation (Phe; 100μM). α1-AR stimulated cells were incubated with a series of inhibitors: prazosin, Praz (1μM); protein kinase C, PKC (1.5μM Ro-31-8220 or 1.25μM rottlerin), ERK (25μM PD98059), p38 (10μM SB203580), SRC (10μM PP2) and JAK2 (25μM AG490). *Statistically significant p≤0.05 from Glu−. #Statistically significant p≤0.05 from Glu−-Phe. N = 5 independent experiments performed in triplicate.