The Protective Effect of Melatonin on Neural Stem Cell against LPS-Induced Inflammation

Figure 6

The measurement of PI3K/Akt/Nrf2 signaling after melatonin treatment in LPS-induced inflammation. (a) Western blotting experiments showed that the relative protein expression of PI3K decreased in the LPS (100 ng/mL) treatment group compared to the normal control group. The relative level of PI3K was elevated in the LPS (100 ng/mL) plus melatonin (100 nM) treatment group compared to the LPS only treatment group. (b) Western blot analyses showed that the relative protein level of Akt decreased in the LPS (100 ng/mL) treatment group compared to the normal control group. The relative level of Akt was elevated in the LPS (100 ng/mL) plus melatonin (100 nM) treatment group compared to the LPS only treatment group. (c) Western blot analyses showed that the relative protein level of Nrf2 decreased in the LPS (100 ng/mL) treatment group compared to the normal control group. The relative level of Nrf2 was elevated in the LPS (100 ng/mL) plus melatonin (100 nM) treatment group compared to the LPS only treatment group. (d) Western blot analyses showed that the relative protein level of Nrf2 decreased in the melatonin (100 nM) treatment group compared to LPS (100 ng/mL) treatment group. Also, the relative level of Nrf2 was also attenuated in the LPS (100 ng/mL) plus melatonin (100 nM) treatment group. In all groups, NSCs were treated with 100 nM wortmannin (a PI3K inhibitor) at 3 hr before melatonin or/and LPS treatment. β-Actin was used as an internal control. Data were expressed as mean ± S.E.M, and each experiment included 4 repeats per condition. Differences were considered significant at , (compared to the control group).

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