Fig 2: Cerebral-IPC protects against MCAO/R injury. (A, C) Representative images of TTC staining showing infarcted regions in the brains in the differentially treated mice. (B) Representative images of HE and Nissl staining showing tissue structure and neuronal density in the differentially treated mice. (D) NDS in the differentially treated mice. (E) Representative immunoblot showing expression levels of COX2, MMP-2, MMP-9, cleaved caspase-1, and cleaved caspase-3 in the indicated groups. F: Representative immunoblot showing expression levels of JNK. P-JNK, p38, p-p38, BAX, and Bcl-2 in the indicated groups. (G, H) Representative images of TUNEL-stained tissues indicating apoptotic cells. (* and # P < 0.05 compared to Sham group and MCAO group, respectively; CIPC: cerebral-IPC; Scale bars: 500 µm for ×40 and 100 µm for ×200)

Fig 3: AET inhibited ER stress and cell apoptosis in the infarcted heart. A and B, Expression of GRP78, CHOP, JNK and caspase12 in the heart was examined with Western blotting; C, Cell apoptosis in the heart was detected by TUNEL staining (green), the nuclei were labeled by DAPI (blue). D, Analysis of the percentages of TUNEL-positive cells in each group. Values were expressed as mean ± SEM, n = 5, Scale bar = 50 µm.

Fig 4: DHA inhibits RANKL-induced NFATc1, NF-?B and MAPK activation in osteoclastogenesis. RAW264.7 cells transfected with NFATc1 and NF-?B were pretreated with various concentrations of DHA for 1 h, and subsequently incubated with a-MEM containing 30 ng/ml M-CSF and 50 ng/ml RANKL for 6 h to activate NF-?B, and 24 h to activate NFATc1. Luciferase activities of (A) NFATc1 and (B) NF-?B were quantitatively analyzed. BMMs were pretreated with or without DHA (5 µM) for 4 h, and then stimulated with 30 ng/ml M-CSF and 50 ng/ml RANKL for the indicated time periods (0, 10, 30 and 60 min, and 0, 1, 3 and 5 days), before the cell lysates were quantitatively analyzed using western blotting for the (C and D) NFATc1, (E and F) NF-?B and (G and H) MAPK signaling pathways. n=3 per group. *P<0.05, **P<0.01 and ***P<0.001 vs. 0 µM control group. DHA, dihydroartemisinin; RANKL, receptor activator of nuclear factor ?B ligand; NFATc1, nuclear factor of activated T cell cytoplasmic 1; NF-?B, nuclear factor ?B; MAPK, mitogen-activated protein kinase; a-MEM, a modified Eagle's medium; M-CSF, macrophage-colony stimulating factor; BMMs, bone marrow derived macrophages; ERK, extracellular regulated protein kinases; JNK, c-Jun N-terminal kinase; p-, phosphorylated.

Fig 5: Hypothetical mechanism through which miR-483-5p attenuates ischemia?reperfusion injury after cardiopulmonary resuscitation. miR-483-5p promotes mitochondrial biogenesis and reduces apoptosis via the TNFSF8/AMPK/JNK pathway