Background and Aim: Regarding the importance of new treatments to control and treat multiple sclerosis (MS), in this study we investigated the role of Benzoaric acid (BA) on the neuro-inflammation and apoptosis processes in the cuprizone (cup)-induced animal model of MS. Materials and Methods: In this experimental study, 35 males C57BL/6 mice were divided into five groups. The study groups were included, control: received six weeks of normal powdered food beside intraperitoneal (i. p. ) injection of BA solvent (100 μ L per day PBS) for the last two weeks, cup: received six weeks of powdered food contains 0. 2% cup beside i. p. injection of BA solvent for the last two weeks and cup-treatment: received six weeks of powdered food contains 0. 2% cup beside i. p. injection of 20, 40 and 80 mg/kg BA for the last two weeks. Eventually, the medial corpus callosum area of the animal’ s brain was evaluated via western blot and Real-Time PCR methods. Ethical Considerations: Ethical points were observed according to the declaration of Helsinki and relevant code of ethics, regarding minimizing harms during animal experimentation (UOZ-GR-9517-13). Findings: Molecular studies have shown that BA-80 decreased mRNA (p <0. 01) and protein expression of NF-KB and consequently increased I-KB/NF-KB ratio (p <0. 05) and decreased inflammation in compare to cup group. Moreover, BA-80 decreased caspase-9 mRNA (p<0. 01) and caspase-8 mRNA (p <0. 05) and subsequently increased caspase-8/caspase-9 ratio (p<0. 01) and decreased apoptosis in compare to cup group. Conclusion: The dose of 80 mg/ml BA via decreasing cup-induced neuro-inflammation and neuro-apoptosis has protective effects in this model.

Purpose: Effect of lipocalin 2 on the expression of heme oxygenase I , II and NF-kB transcription factor was the purpose of this survey.Materials and Methods: Lcn2 was cloned to pcDNA3.1 plasmid by using genetic engineering method. The recombinant vector was transfected to CHO and HEK293T to establish stable cell expressing lipocalin 2. The presence of lipocalin 2 gene in these cells was confirmed by using through RT-PCR and western blot analysis. Expression of Lcn2 was also down-regulated by siRNA in A549 cell line. Expression of of heme oxygenase I , II and NF-kB transcription factor were determined in both ectopic expression Lcn2 cells and Lcn2 down regulated cells by using of RT-PCR and western blot analysis. Results: The results showed that the expression of heme oxygenase I and those of NF-kB were higher in cells expressing recombinant lipocalin2 compared with the control cells. On the other hand, expression of heme oxygenase I and NF-kB in siRNA transfected cells was down-regulated.Conclusion: These findings indicate that lipocalin2 induces the expression of HO-1 and suggest Lcn2 through NF-kB induces HO-1 expression.

Background: Activation of IKK/NF-kB signaling pathway plays a critical role in inflammation-driven tumor progression. Several natural compounds able to inhibit the IKK/NF-kB activation pathway have been shown to either prevent cancer or inhibit cell growth. Extensive studies have been carried out on the Nigella sativa (N. sativa) by many researchers, and its pharmacological activities including anticancer, analgesic, and anti-inflammatory functions have been explored. This study investigated the effect of N. sativa extract on the mRNA level of NFk (p50, RelB) and IKK (IKKA, IKKB) to determine one of the anti-inflammatory mechanisms of N. sativa in breast cancer cells. Methods: In this experimental study, MCF7 cell line was treated with different concentrations of hydroalcoholic extracts of N. sativa (0, 200, 400, 600, 800 μ g/mL) for 24, 48 and 72 h. Effects of the extract on cell viability and NFk (p50, RelB ) and IKK (IKKA, IKKB) gene expression were analyzed by MTT assay and real time PCR, respectively. Results: mRNA expression levels of NFk (p50, RelB) and IKK (IKKA, IKKB) in the treatment group were lower than the untreated (control) group. Fold difference (p50, RelB) of gene expressions in treatment groups were statistically significant (P =0. 001 and P =0. 003) and the fold difference of IKK (IKKA, IKKB) in the treatment groups was lower than that of the untreated groups (P=0. 01 and P=0. 001). Conclusion: One possible anti-inflammatory mechanism of N. sativa is associated with the reduction in mRNA levels of NFk (p50, RelB) and IKK (IKKA, IKKB) in breast cancer.