Different Sources of Dietary Magnesium Supplementation Reduces Oxidative Stress by Regulation Nrf2 and NF-κB Signaling Pathways in High-Fat Diet Rats.
Cemal OrhanBesir ErPatrick Brice Defo DeehAhmet Alp BilgicSara Perez OjalvoJames Richard KomorowskiKazım ŞahinPublished in: Biological trace element research (2021)
Magnesium (Mg) is an essential mineral required for many physiological processes, including ionic balances in ocular tissues. We compared the effects of different Mg-chelates (Mg oxide, MgO vs. Mg picolinate, MgPic) on retinal function in a high-fat diet (HFD) rats. Forty-two rats were divided into six groups and treated orally for 8 weeks as follows: Control, MgO, MgPic, HFD, HFD + MgO, and HFD + MgPic. Mg was administered at 500 mg of elemental Mg/kg of diet. HFD intake increased the levels of retinal MDA and NF-κB, INOS, ICAM, and VEGF but downregulated Nrf2. However, in rats supplemented with MgO and MgPic, the retinal MDA level was decreased, compared with the control and HFD rats. Activities of antioxidant enzymes (SOD, CAT, and GPx) were increased in HFD animals given Mg-chelates (p < 0.001), MgPic being the most effective. Mg supplementation significantly decreased the expression levels of NF-κB, INOS, ICAM, and VEGF in HFD rats while increasing the level of Nrf2 (p < 0.001). Mg supplementation significantly decreased the levels of NF-κB, INOS, ICAM, and VEGF and increased Nrf2 level in HFD rats (p < 0.001), with stronger effects seen from MgPic. Mg attenuated retinal oxidative stress and neuronal inflammation and could be considered as an effective treatment for ocular diseases.
Keyphrases
- high fat diet
- oxidative stress
- adipose tissue
- insulin resistance
- signaling pathway
- optical coherence tomography
- dna damage
- diabetic rats
- diabetic retinopathy
- induced apoptosis
- pi k akt
- lps induced
- metabolic syndrome
- nuclear factor
- skeletal muscle
- gene expression
- cell death
- body mass index
- inflammatory response
- weight loss
- cell cycle arrest
- brain injury
- weight gain
- endoplasmic reticulum stress