Anti-Sod2 polyclonal antibody

Long-term (18 h) preincubation with an antioxidant alpha-tocopherol (alpha-T) both at micromolar and nanomolar concentrations was shown to increase the viability of the PC12 neuronal cell line exposed to oxidative stress, while during short-term preincubation (30 min) alpha-T exhibited a protective effect only at micrimolar concentrations. Using real-time polymerase chain reaction (RT-PCR), it was demonstrated that exposure of PC12 cells to a pro-oxidant hydrogen peroxide increases expression of a proapoptotic mitochondrial protein Bax to a larger extent than that of a antiapoptotic protein Bcl-xL. In contrast, preincubation of PC12 cells with alpha-T before exposure to hydrogen peroxide increased Bcl-xL expression but did not influence Bax expression. Hence, it appears that alpha-T promotes normalization of the Bax/Bcl-xL ratio increased due to the prooxidant's effect. In control PC12 cells, alpha-T significantly increased expression of the transcription factors NRF-2 and TFAM, but not NRF-1, which perform varied functions and, specifically, can activate mitochondrial biogenesis. In addition, alpha-T decreased the Bax/Bcl-xL ratio in PC12 cells, as shown by immunoblotting. At the same time, both exposure to hydrogen peroxide and preincubation with alpha-T caused no significant changes in NRF-1, NRF-2 and TFAM expression in PC12 cells. Preincubation of PC2 cells with alpha-T before exposure to hydrogen peroxide evoked earlier expression of an antiapoptotic enzyme superoxide dismutase 2 (SOD2) than when the prooxidant acted alone. Thus, it appears that normalization of the Bax/Bcl-xl ratio and a relatively early increase in SOD2 expression contribute to the protective effect of alpha-T towards PC12 cells during oxidative stress. The fact that alpha-T increases NRF-2 and TFAM expression in control PC12 cells suggests that alpha-T can slightly boost mitochondrial biogenesis. However, under oxidative stress conditions, which are characterized by a deficiency of macroergic compounds, no evidence for the alpha-T-induced activation of such an energy-consuming process as mitochondrial biogenesis in PC12 cells was found.

Mulberry leaf is a vegetable used in daily diet. It can bring delicious taste and multiple health benefits. However, the chemicals responsible for these health benefits remain unveiled. In this work, two novel prenylated flavonoids were isolated from mulberry leaf. Their structures were identified and named as morachalcone D and morachalcone E. The protective effects of these two compounds were investigated, against endogenous oxidative damage (oxytosis/ferroptosis) induced by glutamate and erastin in HT22 cells. The results revealed that morachalcone D was much more potent in preventing from glutamate- and erastin-induced cell death than morachalcone E. The neuroprotective effect of morachalcone D was related to the prevention of ROS production, glutathione depletion, and iron accumulation. Morachalcone D upregulated the expression of genes involved in antioxidant defense, including GPx4, CAT, SOD2, Nrf2, HMOX1 and SLC7A11. These findings indicated that morachalcone D was responsible for the health benefits of mulberry leaf, and could be a potent neuroprotective agent for use in dietary supplements and functional foods.