The Anti-inflammatory Effect of Ginger Extract on the Animal Model of Multiple Sclerosis.

Background: Experimental autoimmune encephalomyelitis (EAE), as an autoimmune disease in the central nervous system (CNS), is an animal model for multiple sclerosis (MS) mediated by T lymphocytes. Objective: To investigate ginger extract's effect on reducing inflammation and improving the symptoms in the EAE model. Methods: The EAE was induced by injecting MOG35-55 and pertussis toxin into eight-week-old female C57BL6 mice. The mice were treated with an intraperitoneal injection of 300 mg/kg/day of hydroalcoholic extract of ginger for 21 days. The disease severity and weight changes were measured daily. Then, the mice spleens were removed; the gene expressions of interleukin (IL)-17, transforming growth factor beta (TGF-ß), interferon-γ (IFN-γ), and tumor necrosis factor α (TNF-α) were analyzed by Real-time PCR and the percentage of regulatory T lymphocytes (Treg cells) was determined by flow cytometry. Serum nitric oxide and antioxidant capacity were measured, and brain tissue sections were prepared to investigate the leukocyte infiltration and plaque formation. Results: The severity of symptoms in the intervention group was lower than in the control. The gene expression levels of inflammatory cytokines, including IL-17 (P=0.04) and IFN-γ (P=0.01), were reduced. The Treg cells increased significantly, and the serum nitric oxide level was lower in the ginger-treated group. There was no significant difference in lymphocyte infiltration in the brain between the two groups. Conclusion: The present study indicated that ginger extract could effectively reduce inflammatory mediators and modulate immune responses in EAE.

Improving the endothelial dysfunction in type 2 diabetes with chromium and vitamin D3 byreducing homocysteine and oxidative stress: A randomized placebo-controlled trial.

BACKGROUND: Chromium picolinate (CrPic) and vitamin D3 are known as two antioxidant micronutrients. Through inducing endothelial dysfunction, oxidants such as homocysteine (Hct) and malondialdehyde (MDA) lead to cardiovascular disease in type 2 diabetes mellitus (T2DM). No published data has directly examined the effects of these two antioxidants on improving the endothelial dysfunction in T2DM throughreducing homocysteine and oxidative stress. METHODS: Subjects (n = 92) in this randomized, double blind, placebo-control study were randomly assigned to receive oral placebo (group I), D3 (group II: 50,000 IU/ week), chromium picolinate (CrPic) (group III: 500 µg/day), and both vitamin D3 and CrPic (group IV) for four months. Fasting blood samples were drawn at study baseline and following intervention to determine Hct, MDA, total antioxidant capacity (TAC), total thiol groups (SHs), vascular cell adhesion molecule- 1 (VCAM-1), and plasminogen activator inhibitor-1 (PAI-1). RESULTS: After intervention, MDA significantly decreased in groups II and IV; TAC significantly increased in group IV, and SHs significantly augmented in group III; Hct was significantly reduced in groups II, III, and IV; and VCAM-1 significantly decreased in groups III and IV and PAI-1 was significantly reduced in groups II, III, and IV. CONCLUSION: Our findings suggest that through reducing homocysteine and oxidative stress and improving endothelial dysfunction, chromium and vitamin D3 co-supplementation might be predictive and preventive of cardiovascular diseasesassociated with T2DM. IRCT, IRCT20190610043852N1, registered 21 October 2019, https://fa.irct.ir/user/trial/42293/view.

The effects of chromium and vitamin D3 co-supplementation on insulin resistance and tumor necrosis factor-alpha in type 2 diabetes: a randomized placebo-controlled trial.

The current study was conducted to assess the effects of simultaneous usage with vitamin D3 and chromium picolinate (CrPic) supplementations on homeostasis model assessment of insulin resistance (HOMA-IR), fasting blood glucose (FBS), hemoglobin A1c (HbA1c), tumor necrosis factor-α (TNF-α), and lipid profile in type 2 diabetes mellitus (T2DM). Ninety-two patients with T2DM were randomly allocated to the following 4 groups for 4 months: (I) placebo of vitamin D3 (n = 23); (II) vitamin D3 supplement at a dose of 50 000 IU/week (n = 23); (III) CrPic supplement at a dose of 500 µg/day (n = 23); and (IV) both vitamin D3 at a dose of 50 000 IU/week and CrPic at a dose of 500 µg/day (n = 23). HOMA-IR levels increased significantly in groups I and II after the intervention. However, this increase in group I was significantly higher than that in group II after the treatment. HOMA-IR levels were controlled in groups III and IV during the intervention. TNF-α decreased significantly in groups II, III, and IV after the intervention. FBS, HbA1c, and lipid profile did not change significantly in total groups after the intervention. It seems that chromium and vitamin D3 co-supplementation are probably effective in controlling HOMA-IR by decreasing TNF-α in T2DM. Novelty Chromium alone and/or in simultaneous pretreatment with vitamin D3 is more effective than vitamin D3 in controlling HOMA-IR in T2DM. Chromium and vitamin D3 alone and/or in simultaneous pretreatment decrease TNF-α in T2DM.