Lactobacillus plantarum And Inulin: Therapeutic Agents to Enhance Cardiac Ob Receptor Expression and Suppress Cardiac Apoptosis in Type 2 Diabetic Rats.

BACKGROUND: T2DM may cause increased levels of oxidative stress and cardiac apoptosis through elevated blood glucose. The present study investigated the effects of Lactobacillus plantarum (L. plantarum) as a probiotic strain and inulin as a prebiotic supplement on cardiac oxidative stress and apoptotic markers in type 2 diabetes mellitus (T2DM) rats. METHODS: A high-fat diet and a low dose of streptozotocin were used to induce type 2 diabetes. The rats were divided into six groups which were supplemented with L. plantarum, inulin, or their combination for 8 weeks. RESULTS: The results showed improved activity of cardiac antioxidant parameters including total antioxidant capacity (TAC), superoxide dismutase (SOD), and glutathione peroxidase (GPx) (P < 0.001, P < 0.01, and P < 0.01, respectively) and decreased level of cardiac malondialdehyde (MDA) concentration (P < 0.05). These changes were accompanied with increased protein expression of cardiac obesity receptor (Ob-R) (P = 0.05) and reduced apoptotic markers such as tumor necrosis factor-alpha (TNF-α), Fas ligand (FasL), and caspase proteins (P < 0.001, P = 0.003, and P < 0.01, respectively) in T2DM rats after concurrent L. plantarum and inulin supplementation. Moreover, a remarkable correlation of cardiac Ob-R and oxidative stress parameters with cardiac apoptotic markers was observed (P < 0.01). CONCLUSION: The concurrent use of L. plantarum and inulin seems to be beneficial, as they can lead to decreased heart complications of T2DM via reducing cardiac apoptotic markers.

The impact of vitamin D3 intake on inflammatory markers in multiple sclerosis patients and their first-degree relatives.

BACKGROUND & AIMS: In our previous study, a Seesaw model was proposed for the fluctuation of crucial anti- (IL-10) and pro-inflammatory (Il-6 & IL-17A) cytokines through vitamin D3. In this paper, however, it is intended to extend the mentioned model by assessing the expression mRNA levels of IL-27 and TGF-ß1 as well as the changes of plasma levels of IL-27, TGF-ß1, IL-17A, IL-10, and IL-6 after treatment by vitamin D3. METHOD: Venous blood samples were drawn from Healthy Participants (HP, n = 25) and First-Degree Relative Participants (FDRP, n = 25) as control groups and Multiple Sclerosis Participants (MSP, n = 25) before and after eight weeks of supplementation with 50000 IU vitamin D3. The mRNA expression and plasma concentrations were gauged by using Real-Time PCR and ELISA assay, respectively. RESULTS: The mRNA surfaces of IL-27, as well as TGF-ß1, were up-regulated. However, the plasma levels of TGF-ß1, IL-17A, and IL-6 were significantly different among the three groups. In addition, the plasma levels of IL-27, TGF-ß1, IL-10, IL-17A, and IL-6 significantly changed following the administration of vitamin D3. CONCLUSION: The findings of this paper illustrate that anti-inflammatory cytokines could have a key role in immunomodulatory functions due to their anti-inflammatory functions. To conclude, this might contribute to preventing the pathophysiological process of MS. Also, the proposed model could be used as a preventive way on disposed people to multiple sclerosis, particularly in first degree relatives of these patients.

Anti-inflammatory effects of dietary vitamin D3 in patients with multiple sclerosis.

OBJECTIVE: To assess the effects of dietary vitamin D3 on proinflammatory (interleukin-17A [IL-17A] and IL-6) and anti-inflammatory (IL-10) cytokines. METHODS: Our study was conducted on 75 participants who were divided into 3 groups: multiple sclerosis participants (MSPs, n = 25), first-degree relative participants (FDRPs, n = 25), and healthy participants (HPs, n = 25). All groups received 50,000 IU vitamin D3/wk for 8 weeks. Serum 25-(OH) vitamin D3 levels and messenger RNA (mRNA) expression levels of ILs were determined using electrochemiluminescence assay and real-time PCR, respectively. RESULTS: Vitamin D3 affected the levels of IL-17A, IL-10, and IL-6 among the 3 groups (p < 0.001 for all). Levels of IL-17A (MSPs: fold change [FC] = 5.9, p = 0.014; FDRPs: FC = 5.2, p = 0.006; HPs: FC = 4.2, p = 0.012) and IL-6 (MSPs: FC = 5.6, p = 0.003; FDRPs: FC = 5.5, p = 0.002; HPs: FC = 5.1, p < 0.001) were downregulated after vitamin D3 treatment. In addition, levels of IL-10 (MSPs: FC = 6.2, p = 0.005; FDRPs: FC = 4.6, p < 0.001; HPs: FC = 5.2, p < 0.001) were upregulated after 8 weeks. CONCLUSIONS: Although supplementation with vitamin D3 reduced the mRNA expression levels of IL-17A and IL-6, it increased the mRNA expression level of IL-10 in all groups. However, these effects were more considerable in the MSP group than in the other groups. Of interest, in a deficiency state of serum vitamin D3, IL-17A expression had a positive feedback effect on the expression of IL-6. Conversely, in the sufficient state, IL-10 expression had a negative feedback effect on the expression of IL-17A and IL-6.