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.