Propofol (2, 6-diisopropylphenol), is an anesthetic and routinely used for the humans sedation during surgery. The potent inducers of phase II detoxifying and antioxidant stress responsive to propofol were investigated. First, a dose of 25-100 µM propofol showed no significant cytotoxicity on SH-SY5Y cells and pre-treatment of SH-SY5Y cells with propofol (25-100 μM) for 8h prevented cell death and maintained cell integrity following exposure to 1 mM hydrogen peroxide by MTT assays. Then, an increase in the generation of ROS following hydrogen peroxide treatment was significantly attenuated by 8 h pre-treatment with propofol. Additionally, the potential roles of ERK, p 38 MAPK and JNK in the regulation of propofol-induced endogenous HO-1 expression in SH-SY5Y cells were estimated by Western blotting assays. Results showed that propofol significantly increased the phosphorylation levels of ERK, p 38 MAPK and JNK and antioxidant stress responsive to propofol was attenuated by the inhibition of ERK signaling biochemical inhibitors. These results suggest that the ERK pathway plays an important role in the regulation of propofol-mediated antioxidant effects in SH-SY5Y cells.

In the present study, the potent inducers of phase II detoxifying and antioxidant stress responsive to icariside II was investigated. First, a dose of 0–10 µM icariside II showed no significantly cytotoxicity on HepG2 cells by MTT assays and icariside II could enhance cellular GSH levels by ELISA assay. Then, the potential roles of ERK, Akt and JNK in the regulation of icariside II-induced Nrf2-dependent ARE transcriptional activity as well as ARE-mediated endogenous HO-1 and glutathione GST protein expression in HepG2 cells were estimated. Icariside II activated the nuclear translocation of Nrf2 and the up-regulated expression of Nrf2-related antioxidant protein OH-1 and GST were evaluated by Western blotting. Then the phosphorylation levels of ERK1/2, Akt and JNK1/2 were further examined by Western blotting assays. Results showed that icariside II significantly increased the phosphorylation levels of ERK1/2, Akt and JNK1/2. Furthermore, icariside II-induced ARE transcriptional activity was attenuated by the inhibition of ERK, Akt and JNK signaling using biochemical inhibitors. These results suggest that the Nrf2/ARE pathway plays an important role in the regulation of icariside-mediated antioxidant effects in HepG2 cells.

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These findings suggest that SGB could have antioxidative effects against AMI, and the protective effect of right SGB was more effective than that of left SGB. Thus, the right SGB could be an effective and safe method of local anesthesia to protect against cardiac damage due to oxidative stress.