Skip to main content
. 2025 Mar 4;6(3):e70110. doi: 10.1002/mco2.70110

FIGURE 7.

FIGURE 7

Nilvadipine reversed cholestatic liver injury induced by dexamethasone or PDE in female offspring rats with long‐term efficacy. (A) GRP78 and CHOP mRNA expression. (B) GRP78 and CHOP protein expression by western blot. (C, D) GRP78 and CHOP protein expression by immunofluorescence (400×). (E) Cholestatic liver injury‐related indicators. (F) The relative luciferase activities. (G, K) Liver injury‐related indicators level at PW12 and PW28. (H, L) Cholestasis‐related indicators level at PW12 and PW28. (I, M) Liver 27‐hydroxycholesterol contents at PW12 and PW28. (J, N) GRP78 and CHOP protein expression at PW12 and PW28. A–G was detected in human WJ‐MSCs after being treated with DEX and/or nilvadipine. Data are shown as the mean ± SEM, n = 3 for western blot and immunofluorescence, n = 10 for detecting the related serum indicators, n = 6 for other experiments. * p < 0.05, ** p < 0.01 vs. control; # p < 0.05 vs. DEX or PDE group. PDE, prenatal dexamethasone exposure; GRP78, glucose‐regulated protein 78; CHOP, C/EBP homologous protein; GAPDH, glyceraldehyde‐3‐phosphate dehydrogenase; PW, postnatal week; DEX, dexamethasone; ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; GGT, glutamyl transpeptidase; TBI, total bilirubin; DBI, direct bilirubin; TBA, total bile acid; WJ‐MSCs, Wharton's Jelly derived mesenchymal stem cells; DEX, dexamethasone.