The protective effect of rifampicin on behavioral deficits, biochemical, and neuropathological changes in a cuprizone model of demyelination.

Multiple sclerosis (MS) is a disease of the central nervous system (CNS) in which both neuroinflammation and neurodegeneration play critical roles in the pathogenesis of the disease. A growing body of evidence indicates that some antibiotics have anti-inflammatory and neuroprotective properties. Rifampicin, commonly used for the treatment of mycobacteria, has been shown to exert neuroprotective activities in neurodegenerative diseases. In this study, we examined the efficacy of rifampicin on demyelination, gliosis, apoptosis, inflammation, behavioral dysfunction, and biochemical alterations in the cuprizone model of demyelination. For this aim, male C57BL/6J mice were fed a chow containing 0.2% cuprizone (w/w) for 6 weeks to induce reversible demyelination in the corpus callosum. Mice intraperitoneally received serial doses of rifampicin (10, 20, or 40 mg/kg body weight) in the last 7 days of a 6-week period of cuprizone treatment. The results showed that the administration of rifampicin led to the improvement in motor behavioral deficits. In line with this, rifampicin decreased the number of apoptotic cells in the corpus callosum thereby diminishing the expression of cleaved caspase-3 and Bax, as well as increasing Bcl-2. Moreover, rifampicin significantly lowered the levels of interleukin-6, interleukin-1ß, caspase-12 activity, heme oxygenase-1(HO-1), nitric oxide (NO), and malondialdehyde (MDA) in mice treated with cuprizone. Conversely, the activity of glutathione peroxidase (GPx) and the level of ferric reducing ability of plasma (FRAP) were increased in response to the treatment with rifampicin. Histopathological findings demonstrated that rifampicin statistically promoted remyelination and mitigated microgliosis and astrogliosis. It seems that rifampicin is able to be added to the armamentarium of therapies for multiple sclerosis.

The effects of nutrition bio-shield superfood powder on immune system function: A clinical trial study among patients with COVID-19.

The present study aimed to evaluate the effects of Nutrition Bio-shield Superfood (NBS) powder on the immune system function and clinical manifestations in patients with COVID-19. We compare the effects of NBS powder on the immune system function and clinical manifestations among two different groups: 1) intervention group receiving standard treatment scheduled according to treatment guidelines plus NBS powder, and 2) control group receiving only the same standard treatment. The serum levels of IL-2, IL-6, IL-17, IFNγ, and TNFα were determined after four weeks of treatment by specific ELISA kits according to the manufacturer's instructions. Finally, the level of immune system stimulation and inflammatory markers were compared at baseline and after intervention in both groups. Data were analyzed using SPSS (version 22). A p-value of ≤ 0.05 was set as significant. A total of 47 patients with COVID-19 (24 patients in the intervention group and 23 patients in the control group) were included in this study. Results showed that the differences in the mean decrease of IL-2, IL-6, and TNF-α in the intervention group in comparison to the control group were 0.93, 10.28, and 8.11 pg/ml, respectively (P<0.001). On the other hand, there was no difference in IL-17, IFNγ, monocytes, eosinophil, and other inflammatory indices between the intervention and control groups. Although NBS powder was able to significantly decrease the levels of some proinflammatory cytokines in patients with COVID-19, however, it is noteworthy that the course of the disease was to large part unaffected by NBS power and there was a reduction independent of treatment. The present study indicates that NBS powder could provide a beneficial anti-inflammatory effect in patients with COVID-19. Hence, NBS in treating patients with COVID-19 shows promise as an adjuvant to the current standard antiviral treatment of such patients. Clinical Trial Registration: https://www.irct.ir, identifier IRCT20200426047206N1.