[Retracted] Chrysophanol Ameliorates Hemin-Induced Oxidative Stress and Endoplasmic Reticulum Stress by Regulating MicroRNA-320-5p/Wnt3a Pathway in HT22 Cells

Figure 1

Chrysophanol (CHR) prevented HT22 cell survival, antiapoptosis, and anti-ER stress in hemin-induced HT22 cell injury models. (a) Cell viability was studied for nonhemin (0 μM) and hemin (20 μM)-treated HT22 cells dealt with varying concentrations of CHR (0, 5, 10, 20, and 40 μM; treatment time: 24 h) by conducting CCK-8 assays. vs. nonhemin. ^## and ^### vs. hemin. . (b) Expression of PCNA affected by CHR in hemin-induced HT22 cells was detected using the western blot. ^N.S. and . . (c) LDH release level was analyzed in nonhemin (0 μM) and hemin (20 μM)-treated HT22 cells in the presence and absence of CHR (0, 5, 10, 20, and 40 μM; treatment time: 24 h) by conducting the LDH cytotoxicity assay. ^N.S. and . . (d) Caspase-3 activity was studied in hemin-induced cells in the presence and absence of CHR (10 μM). . (e) Rate of cell apoptosis was determined using hemin-induced cells in the presence and absence of CHR (10 μM; treatment time: 24 h) by conducting TUNEL staining assays.  μm, . . (f) The protein expression levels of apoptosis-related genes (cleaved caspase-3, Bax, and Bcl-2) were analyzed in hemin-induced cells in the presence and absence of CHR (10 μM; treatment time: 24 h) using the western blot technique. , , and . . (g) Levels of protein expression of ER stress-related genes (p-eIF2α, CHOP, GRP78, and cleaved caspase-12) were analyzed in hemin-induced cells in the presence and absence of CHR (10 μM; treatment time: 24 h) using the western blot technique. and . .

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