Figure 7.

ER stress and Nrf2 regulation in Baicalin-mediated protection. We used ER stress inhibitor tauroursodeoxycholic acid dihydrate (TUDCA) (100 μM), ER stress inducer Tm (2.5 μg/mL), Nrf2 inhibitor brusatol (80 μM) and Nrf2 inducer tert-butylhydroquinone (t-BHQ) (40 μM) in combination with Baicalin pretreatment to study the role of ER stress and Nrf2 in Baicalin-mediated protection. Western blot analysis proved their effects on ER stress and Nrf2 expression (B); We then compared the cell viability between different groups (A). There was no significant difference between Baicalin pretreatment with TUDCA or the t-BHQ group and the Baicalin pretreatment alone group. These three groups both have higher cell viability than the cell viability in the H₂O₂ group. However, Baicalin pretreatment with Tm or brusatol did not exert protective effects against H₂O₂-induced injury. These two groups did not have higher cell viability than the cell viability in the H₂O₂ group. *** p < 0.001 vs. the group with H₂O₂ treatment, n = 6.