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

Figure 3

CHR inhibited HT22 cell apoptosis, ER stress, and oxidation stress by downregulating miR-320-5p in hemin-induced HT22 cell injury models. NC mim.: negative control mimics; miR mim.: miR-320-5p mimics. (a) Volcano plot generated for the miRNA expression profiles for the hemin-induced HT22 cell injury and CHR treatment groups. (b) Levels of expression of the top six miRNAs with the most significant difference in expression (identified following the sequencing method) were studied using hemin-induced cells in the presence and absence of CHR (10 μM; treatment time: 24 h) using the RT-PCR technique. , , and . . (c) Level of expression of miR-320-5p was studied using hemin-induced cells in the presence and absence of CHR (10 μM; treatment time: 24 h) using the RT-PCR technique. . . (d) The apoptosis rate in hemin-induced HT22 cells in the presence and absence of CHR (10 μM; treatment time: 24 h) or miR-320-5p mimics (treatment time: 24 h) was studied by conducting the TUNEL staining assays. . . (e) Protein expression levels of the ER stress-related genes (p-eIF2α, CHOP, GRP78, and cleaved caspase-12) were analyzed in hemin-induced HT22 cells in the presence and absence of CHR (10 μM; treatment time: 24 h) or miR-320-5p mimics (treatment time: 24 h) using the western blot technique. , , and . . (f) The changes of oxidation stress-related indexes (ROS, MDA, SOD, and GPx) were analyzed in hemin-induced HT22 cells in the presence and absence of CHR (10 μM; treatment time: 24 h) or miR-320-5p mimics (treatment time: 24 h). and . .

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