Fig 2: Effects of Bar pretreatment on the ERS-associated apoptosis pathway following myocardial ischemia reperfusion injury. (A) Representative western blot analysis and (B) quantification of the ERS-associated proteins (a) GRP78, (b) p-PERK, (c) ATF4, (d) CHOP, (e) caspase-12 and (f) caspase-3 from myocardial cell specimens. Expression of GAPDH was used as the loading control. The results were normalized to the percentage of GAPDH expression; n=6. Data are presented as the mean ± standard error of the mean. **P<0.01 compared with the S group; ##P<0.01 compared with the I/R group. Bar, barbaloin; S, Sham operation + DMSO; I/R, ischemia and reperfusion; ERS, endoplasmic reticulum stress; GRP78, glucose regulatory protein 78; p-, phosphorylated; PERK, PKR endoplasmic reticulum kinase; ATF4, transcriptional activator 4; CHOP, C/EBP-homologous protein.

Fig 3: TMTC3 enhanced ER stress by disturbing the interaction between GRP78 and PERK. A. Colocalization of TMTC3 and GRP78 or PERK in cell lines by IF. Scale bar, 30 µm. B and C. Expression of ER sensors in ESCC negative control and Si-TMTC3 (B) or Sh-TMTC3 (C) cells. D and E. Co-immunoprecipitation of TMTC3, GRP78 and PERK in cell lines. F. Co-immunoprecipitation and Western blot analysis for GRP78 and PERK in Sh-TMTC3 or Sh-NC cells.

Fig 4: PCOS-like rat ovarian dysfunction is improved via a combined curcumin and exercise treatment possibly via excessive ER stress suppression. PCOS-like rats received 8 weeks of curcumin gavage, treadmill exercise, and curcumin combined with treadmill exercise treatment. (a) Transmission electron microscopic analysis of follicles from each group (×3.0 k and ×8.0 k). (b–f) The expression of IRE1a, p-IRE1a, XBP1, PERK, ATF-6, GRP-78, and CHOP in ovaries was assessed by western blot and qRT-PCR assay. (g, h) The levels of Bax, cleaved-caspase-3, and caspase-9 by western blot. Three independent experiments were performed with similar results. Data are shown as mean ± SEM. **P < 0.05 vs. Ctrl. ##P < 0.05 vs. PCOS. #&P < 0.05 vs. P+C/P+E.

Fig 5: ORY suppressed AML12 cells from CoCl2- or tunicamycin-induced endoplasmic reticulum stress. (a, b) Western blotting analysis of GRP78, PERK, p-PERK, EIF2S1, p-EIF2S1, CHOP, and ß-actin expressions in cells from the control, ORY, CoCl2, and CoCl2+ORY groups. (c, d) Western blotting analysis of GRP78, p-PERK, p-EIF2S1, CHOP, and ß-actin expressions in cells from the control, ORY, tunicamycin, and tunicamycin+ORY groups. Relative protein abundance was semiquantified by densitometry (n = 3). Data were expressed as mean ± standard deviation (SD) values. *P < 0.05, **P < 0.01, and ***P < 0.001 versus the control group; #P < 0.05, ##P < 0.01, and ###P < 0.001 versus the CoCl2 group.