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. 2020 Aug 3;5(32):19960–19967. doi: 10.1021/acsomega.0c01121

Figure 1.

Figure 1

α-MG ameliorates cisplatin-induced cytotoxicity in HEK293 cells. (A) Chemical structure of α-mangostin (α-MG). α-MG ameliorates cisplatin-induced cytotoxicity in HEK293 cells. (B) Cytotoxicity effects of cisplatin on HEK293 cells. The cells were incubated with 20 μM cisplatin in varying durations (1–24 h). (C) α-MG exerts protective effects against cisplatin-induced decrease in cellular viability. HEK293 cells were pretreated with α-MG (5–40 μM) for 24 h and then exposed to cisplatin for 24 h. (D) Cells were pretreated with α-MG (40 μM) and then cultured in the presence of cisplatin (1–24 h). (E) Cells were incubated with α-MG (5–40 μM) alone for 24 h. Cell viability was measured by the MTT assay. α-MG (0–40 μM) dose-dependently attenuates cisplatin-induced lipid peroxidation in HEK293 cells. (F, G) Levels of (F) GSH and (G) MDA were determined using commercial kits. Cells pretreated with α-MG (0–40 μM) for 24 h attenuate cisplatin-induced accumulation of intracellular ROS. (H) Quantitative analysis of ROS. Data are represented as means ± SD; *p < 0.05, **p < 0.01 compared to the control group; #p < 0.05, ##p < 0.01 compared with the cisplatin group. (I) Representative images indicated the intracellular ROS assay. Green fluorescence shows positive cells. Note: (a) normal group, (b) 40 μM α-MG separate treatment group, (c) cisplatin separate treatment group, (d) 10 μM α-MG and cisplatin coprocessing group, (e) 20 μM α-MG and cisplatin coprocessing group, and (f) 40 μM α-MG and cisplatin coprocessing group.