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. Author manuscript; available in PMC: 2017 May 1.
Published in final edited form as: Mol Cell Biochem. 2016 Mar 29;416(1-2):11–22. doi: 10.1007/s11010-016-2688-z

Fig. 5.

Fig. 5

Initiation of apoptosis by β-alanine treatment. a Western blot analysis of procaspase 3 and cleaved caspase-3 content of whole homogenates of control and β-alanine-treated fibroblasts. The upper panel depicts a representative Western blot for procaspase-3 and cleaved caspase-3 content, with glyceraldehyde 3-phosphate dehydrogenase (GAPDH) serving as a loading control. Data in the lower panel represent mean ± S.E.M of four different preparations. The asterisk denotes a significant difference between control and β-alanine-treated fibroblasts (p < 0.05). b Western blot analysis of procaspase-9 content of whole homogenates of control and β-alanine-treated fibroblasts, with β-actin serving as a loading control. The upper panel depicts a representative gel of procaspase-9 content. Data in the lower panel represent mean ± S.E.M of four different preparations. The asterisk denotes a significant difference between the control and β-alanine-treated fibroblasts (p < 0.05). c. Control and β-alanine-treated fibroblasts were loaded with calcein AM (250 μM) Representative image of control and apoptotic, β-alanine-treated fibroblasts. Control fibroblasts appear elongated with a smooth cell surface, while the apoptotic fibroblasts treated for 48 h with β-alanine appear rounded with budding of apoptotic bodies. d Effect of cyclosporin A (200 nM) on percent of β-alanine-treated cardiomyocytes undergoing apoptosis