Fig 1: QMNPs and/or RT effect on cell cycle, apoptosis, CD4 and CD8: (A) cell cycle analysis, (B) Bcl-2 and caspase-3 expression, (C) CD4 expression, and (D) CD8 expression. Values expressed as the mean ± SEM, n = 5.QMNP indicates quercetin magnetite nanoparticles; RT, radiotherapy; SEM, mean ± standard error.a1P < .001, a2P < .01, a3P < .05 vs control; b1P < .001, b2P < .01 vs tumor group; c1P < .001, c2P < .01, c3P < .05 vs RT group; d2P < .01, d3P < .05 vs QMNPs group.
Fig 2: Effect of cisplatin and other pharmacological agents on the Bcl-2 activity in the heart homogenates. The values are in Mean ± SD.
Fig 3: Proposed mechanism for DMF therapeutic efficacy in managing HD-induced motor dysfunction. DMF ameliorates striatal loss of neurons in a 3-NP induced HD model by 1) inducing AKT/mTOR activation to inhibit intrinsic apoptosis caused by both ER stress arms IRE1a/JNK and PERK/CHOP/GADD153 activation; 2) activating the BDNF/TrkB/AKT/CREB axis to overweigh the pro-survival Bcl-2 and enhance DA formation; 3) downregulating miRNA-634 to initiate AKT activation; and 4) suppressing the oxidative stress response consequent to CHOP/GADD153 inhibition to additionally suppress intrinsic apoptosis. AKT, protein kinase B, Bax, B-cell lymphoma-2-associated X; Bcl-2, B-cell lymphoma-2; BDNF, brain-derived neurotrophic factor; CHOP/GADD153, C/EBP homologous protein; CREB, cAMP response element-binding protein; DA, dopamine; DMF, dimethyl fumarate; DR, dopamine receptor; HD, Huntington’s disease; IRE1a, inositol-requiring enzyme 1 alpha; JNK, c-Jun NH2-terminal kinase; miRNA-634, microRNA-634; mTOR, mammalian target of rapamycin; 3-NP, 3-nitropropionic acid; Nrf2, nuclear factor (erythroid-derived 2)-like 2; PERK, protein kinase R-like endoplasmic reticulum kinase; ROS, reactive oxygen species; TH, tyrosine hydroxylase; TrkB, tropomyosin receptor kinase B. This figure is created in BioRender.com.
Fig 4: Cytoplasmic levels of caspase-3 (A), Bax (B), Bcl2 (C), and cytochrome-c (D) in the left ventricles (LVs) of all rat groups. Data were analyzed with one-way ANOVA followed by Tukey’s test. Values are presented as mean ± SD (n = 8/group). Data were considered significantly different at p < 0.5. a: significantly different as compared to control rats; b: significantly different as compared to AKBA-treated rats; c: significantly different as compared to STZ-diabetic rats; d: significantly different as compared to STZ + AKBA-treated rats. CC–compound C (a selective AMPK inhibitor).
Fig 5: Effect of DMF on the striatal protein expression/content of (A) p-IRE1a; (B) p-JNK1/JNK2, Bcl-2, and Bax; and (C) active caspase-3 in HD rats. Data are represented as mean ± SD (n = 3 rats/group for WB; n = 6 rats/group for ELISA) using one-way ANOVA, followed by Tukey’s post hoc test * vs. CONT and # vs. HD at p < 0.05. Bax, B-cell lymphoma-2-associated X; Bcl-2, B-cell lymphoma-2; CONT, control; DMF, dimethyl fumarate; HD, Huntington’s disease; IRE1a, inositol-requiring enzyme 1 alpha; JNK, c-Jun NH2-terminal kinase.
Supplier Page from MyBioSource.com for Rat Apoptosis regulator Bcl-2 ELISA Kit