α-Tocopherol Effects Antioxidant of Bone Marrow Mesenchymal Cells

Objectives: The role of vitamin E (VE) as an antioxidant is widely accepted, and it is involved in various metabolic systems including the regulation of gene expression and inhibition of cell proliferation. The most predominant isoform of VE in the living body is α-tocopherol. However, the influence of α-tocopherol on bone marrow mesenchymal cells (BMMCs) derived from type II diabetes mellitus (DM) has not been investigated. Therefore, this study investigated the effect and activation mechanism of stimulating BMMCs derived from type II DM with α-tocopherol.
Methods: BMMCs were isolated from the femurs of type II DM rat. The α-tocopherol concentration was 1.0 μM, the normal α-tocopherol concentration was 10 μM and the overdose α-tocopherol concentration was 100 μM. The effect of different α-tocopherol concentrations on BMMCs cell proliferation, H₂O₂ activity, antioxidant and inflammatory cytokine production was measured.
Results: The effect of different α-tocopherol concentrations on BMMCs cell proliferation, H₂O₂ activity, antioxidant and inflammatory cytokine production was measured. α-Tocopherol didn’t promote cell proliferation, but H₂O₂ activity at 100 μM was significantly higher. α-Tocopherol at 10 μM increased the gene expression of IL-1β and especially TNF-α. The expression of catalase at 100 μM was lower than for the other α-tocopherol concentrations. α-Tocopherol concentrations of 10 and 100 μM increased the protein levels of ERK signaling pathway, with the greatest change evident at 10 μM.Expression levels of catalase were high after incubation with 100 μM compared with the other α-tocopherol concentrations.
Conclusions: We suggest that a low α-tocopherol concentration has beneficial effects on GK-BMMCs, and that increasing the α-tocopherol concentration to normal level has adverse effects on GK-BMMCs in terms of and the progress of inflammation. Careful control of the α-tocopherol concentration is important for GK-BMMCs, and it is better to avoid increasing the α-tocopherol concentration in type II DM patients.