Curcumin Protects Human Keratinocytes against Inorganic Arsenite-Induced Acute Cytotoxicity through an NRF2-Dependent Mechanism
Figure 5
The protective effect of curcumin on iAs3+-induced cytotoxicity and apoptosis is dependent on NRF2 activation in HaCaT cells. Protocols for curcumin treatment and arsenic exposure are the same as Figure 4(a). (a) The protein level of NRF2, KEAP1, and HMOX-1 under basal and curcumin-treated condition in scramble, NRF2-KD, and KEAP1-KD cells. Cells were treated with vehicle or 20 μM curcumin for 6 hr. Whole-cell lysates were separated on 4–12% Tris-Glycine gels. Vehicle, medium. (b) The effect of curcumin treatment on iAs3+-induced cytotoxicity in Scramble, NRF2-KD and KEAP1-KD cells. Cell viability was measured by MTT assay. Values are mean ± SD. . * versus curcumin-untreated with the same iAs3+ exposure. (c) Effect of curcumin treatment on iAs3+-induced apoptosis in NRF2-KD and KEAP1-KD cells. Apoptotic cells were determined by flow cytometry. Annexin V-positive cells were quantified as apoptotic cells. . (d) Immunoblotting of cleaved caspase-3, PARP, and cleaved PARP. Vehicle, medium; iAs3+, cells exposed to 30 μM of iAs3+ for 20 hr; Cur + iAs3+, cells treated with 5 μM curcumin for 26 hr and exposed to iAs3+ for 20 hr. Whole-cell lysates were used for analysis and β-actin was used as a loading control.
