The Potential of Glucose Treatment to Reduce Reactive Oxygen Species Production and Apoptosis of Inflamed Neural Cells In Vitro.

Protein levels of CREB, JNK, and p70S6K, rose significantly after glucose treatment ( p < 0.01), and the increase in NF-κB, p38, ERK1/2, Akt, and STAT5 approached significance after glucose treatment ( p < 0.05), implying that glucose stimulated all these cytokines level toward a baseline (less neuroinflamed) condition ( Figure 2 ).

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Compared to the lesion group, we found that glucose treatment enhanced the levels of the mitogen-activated protein kinase (MAPK) subgroups including JNK (significantly), NF-κB, p38, ERK1/2, and Akt (with near significance; p < 0.05), which contribute to anti-apoptosis activity and cell proliferation for survival [ 48 , 49 , 50 ].

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