Fig 1: Effect of mitoxantrone with/without exercise on CSF levels of A Bcl-2, B Bax and C Bcl-2/Bax ratio. Values are presented as mean ± S.D. (n = 6). Comparison inside the same group was done using one-way ANOVA followed by Tukey's Multiple Comparison Test. Comparison between sedentary and exercised groups was done using two-way ANOVA followed by Bonferroni Correction Test (p < 0.05). As compared with CNSED (*), CNEX ($), EAESED (#), EAEEX (%) and exercised vs sedentary rats (ψ). EAE experimental autoimmune encephalomyelitis; groups of CNSED sedentary control, CNEX exercised control, EAESED sedentary untreated EAE, EAEEX exercised untreated EAE, MTSED sedentary mitoxantrone, MTEX exercised mitoxantrone
Fig 2: Levels and mRNA expression levels of the apoptotic proteins (Bcl-2, Bax and caspases-3) in the renal tissue following treatment with PbAc (20 mg/kg) and/or CoQ10 (10 mg/kg). ELISA readings are presented as mean ± SD (n = 7). Real-time PCR results are presented as mean ± SEM of triplicate assays and adjusted to Actb. a indicates significant difference vs. the control group at P < 0.05; b indicates significant difference vs. the PbAc treated group at P < 0.05.
Fig 3: Effect of CRBST 250 and 500 mg/kg on Bax (A); BCL-2 (B); Bax: BCL-2 ratio (C) and A-caspase-3 (D) in rats with AA-induced UC. Results are shown as the mean ± SD (n = 6). **p < 0.01, ***p < 0.001, ****p < 0.0001. Normal, normal control rats administered the vehicle; CRBST 500, normal rats administered carbocisteine (500 mg/kg); UC, AA-induced UC rats administered the vehicle; UC/CRBST 250, AA-induced UC rats treated with carbocisteine (250 mg/kg); UC/CRBST 500, AA-induced UC rats treated with carbocisteine (500 mg/kg).
Fig 4: Time course effect of 2-ME on liver p53 (5A), Bax (5B), Bcl-2 (5C) and caspase-3 (5D) levels. Values are expressed as mean ± standard error of the mean. Bars labeled with different letters are statistically significant (p < 0.05).
Fig 5: Effect of AEA on renal contents of (A) WNT-5A and (B) BCL-2, as well as (C) caspase-3 activity in HgCl2-induced AKI in rats. Data are expressed as the mean of 6 rats ± SD. **P < 0.01 and ***P < 0.001 compared with CONT and @@@P < 0.001 compared with HgCl2 groups using one-way ANOVA followed by Tukey's Multiple Comparison post hoc test. AEA anandamide, AKI acute kidney injury, BCL-2 B-cell lymphoma-2, CONT control, HgCl2 mercuric chloride.
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