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. 2015 Mar 12;13(3):1267–1289. doi: 10.3390/md13031267

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© 2015 by the authors; licensee MDPI, Basel, Switzerland.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Peracetylated chitosan oligosaccharides protect PC12 cells against glutamate-induced loss of MMP and the activation of Caspase-3 and Caspase-9. (A) After being pretreated with 200 μg/mL of different PACO monomers Q-2, Q-3 and Q-4 for 2 h and 4 mM of glutamate for another 24 h, the mitochondrial membrane potential (MMP) in PC12 cells were evaluated with the probe JC-1. Data were expressed as a percentage of non-treated control. Values are the mean ± SD (n = 3). Significance: # p < 0.05 vs. normal control group; * p < 0.05, ** p < 0.01 vs. glutamate treated control group; (B) After being pretreated with 200 μg/mL of different PACO monomers Q-2, Q-3 and Q-4 for 2 h and 4 mM of glutamate for another 24 h, the levels of cleaved caspase-3 were measured by western blot. Blots were also probed for β-actin protein as loading controls. The result shown is a representative of three separate experiments with similar results. (C) Quantification of immunoblot for the ratio of caspase-3 to β-actin. The ratio for non-treated normal control cells was assigned values of 1.0 and the data presented as mean ± SD (n = 3). Significance: ## p < 0.01 vs. normal control group; ** p < 0.01 vs. glutamate treated control group. (D–E) After treatment, the activities of caspase-3 (D) and caspase-9 (E) were measured using an ELISA assay kit (Beyotime, China). Data were expressed as a percentage of non-treated control. Values are the mean ± SD (n = 3). Significance: # p < 0.05 vs. normal control group; * p < 0.05 vs. glutamate treated control group.

Peracetylated chitosan oligosaccharides protect PC12 cells against glutamate-induced loss of MMP and the activation of Caspase-3 and Caspase-9. (A) After being pretreated with 200 μg/mL of different PACO monomers Q-2, Q-3 and Q-4 for 2 h and 4 mM of glutamate for another 24 h, the mitochondrial membrane potential (MMP) in PC12 cells were evaluated with the probe JC-1. Data were expressed as a percentage of non-treated control. Values are the mean ± SD (n = 3). Significance: # p < 0.05 vs. normal control group; * p < 0.05, ** p < 0.01 vs. glutamate treated control group; (B) After being pretreated with 200 μg/mL of different PACO monomers Q-2, Q-3 and Q-4 for 2 h and 4 mM of glutamate for another 24 h, the levels of cleaved caspase-3 were measured by western blot. Blots were also probed for β-actin protein as loading controls. The result shown is a representative of three separate experiments with similar results. (C) Quantification of immunoblot for the ratio of caspase-3 to β-actin. The ratio for non-treated normal control cells was assigned values of 1.0 and the data presented as mean ± SD (n = 3). Significance: ## p < 0.01 vs. normal control group; ** p < 0.01 vs. glutamate treated control group. (D–E) After treatment, the activities of caspase-3 (D) and caspase-9 (E) were measured using an ELISA assay kit (Beyotime, China). Data were expressed as a percentage of non-treated control. Values are the mean ± SD (n = 3). Significance: # p < 0.05 vs. normal control group; * p < 0.05 vs. glutamate treated control group.