Evaluation of the neuroprotective effects of Vitamin E on the rat substantia nigra neural cells exposed to electromagnetic field: An ultrastructural study.

Electromagnetic fields (EMFs) could induce oxidative stress (OS) in human tissues. Lipid peroxidation (LPO) is the main hallmark of OS that harms neural cell components, primarily lipids in the myelin sheaths and membranes. Vitamin E is a lipophilic antioxidant that protects cells from OS-related damages and inhibits the LPO process. In this study, male rats were assigned into three groups of Control, EMF, and EMF+ Vitamin E. The EMF producer equipment produced an alternate current of 50 Hz, 3 Mili Tesla (mT). At the end of the experiment, half of the substantia nigra in every sample was used for measurement of the malondialdehyde (MDA) level as the end-product of the LPO and activity of superoxide dismutase (SOD) enzyme. The next half of the tissue was prepared for transmission electron microscopy (TEM). In the EMF group, MDA level was enhanced and SOD value decreased significantly compared to the control group, but Vitamin E could restore these changes. In rats undergone EMF, heterochromatic nucleus and destruction in some portions of the nuclear membrane were detected. The segmental separation or destruction of myelin sheath lamellae was observed in nerve fibers. In treated animals, the nucleus was round, less heterochromatic, with a regular membrane. Separation of myelin sheath lamellae in some nerve fibers was slighter than the radiation group. Considering the results, EMF exposure induces LPO and triggers ultrastructural changes in the cell membranes, nucleus, and myelin sheath of substantia nigra cells, but Vitamin E consumption weakens these neuropathological alterations.

Indirect coculture of stem cells with fetal chondrons using PCL electrospun nanofiber scaffolds.

In vitro coculture system provides a powerful tool for tissue engineering. In this study, we evaluated the gene expressions of human adipose-derived stem cells (ASCs) on polycaprolactone (PCL) scaffold in coculture model with fetal chondrons. Electrospun PCL scaffolds (900 nm fiber diameter) were created and human infrapatellar fat pad-adipose-derived stem cells (IPFP-ASCs) were seeded on these scaffolds. Scanning electron microscopy (SEM) showed attachment of human IPFP-ASCs to scaffold. IPFP-ASCs on scaffolds were cocultured with fetal chondrons in transwell. Gene expressions were investigated using real-time polymerase chain reaction (real-time PCR). In comparison with control group, the expression level of collagen type 2 and aggrecan were significantly decreased but Indian Hedgehog(IHH) significantly increased (P < 0.05).These findings may interpreted that IPFP-ASCs seeded on PCL scaffold, in cocultures with fetal chondrons are tending toward osteogenesis rather than chondrogenesis.

Protective Effects of Vitamin E Consumption against 3MT Electromagnetic Field Effects on Oxidative Parameters in Substantia Nigra in Rats.

INTRODUCTION: Electromagnetic fields (EMFs) can influence the biological system by the formation of free radicals in cells. The EMFs are able to deteriorate defense system against free radicals that leads to oxidative stress (OS). Lipid peroxidation process (LPO) is an index of oxidative stress, and the Malandialdehyde (MDA) is the final product of LPO. Vitamin E is the most important antioxidant which inhibits the LPO process. The aim of this study was to evaluate the effects of 3MT EMF exposure on oxidative stress parameters in substantia nigra and the role of vitamin E in reducing oxidative stress and preventing of LPO process. METHODS: 40 male Wistar rats were randomly divided into 4 groups: 1) Control group: received standard food without exposure to EMF and without consumption of vitamin E, 2) Experimental group 1: was exposed to EMF (3MT) 4 h/day for 50 days, 3) The experimental group 2: received 200 mg/kg vitamin E with gavage every day and also was exposed to EMF (3MT) 4 h/day for 50 days, 4) Sham group: received water with gavage for 50 days. RESULTS: A significant increase in MDA levels and Glutation peroxidase (GSH-Px) activity of the substantia nigra following 50 days exposure to EMF was detected, but the superoxide dismutase (SOD) activity was decreased. Exposure did not change total antioxidant capacity (TAC) levels in plasma. Vitamin E treatment significantly prevented the increase of the MDA levels and GSHPx activity and also prevented the decrease of SOD activity in tissue but did not alter TAC levels. The GSH-Px activity increased because the duration and intensity of exposure were not enough to decrease it. CONCLUSION: We demonstrated two important findings; that 50 days exposure to 3 MT electromagnetic field caused oxidative stress by increasing the levels of MDA, and decreasing SOD activity in the substantia nigra; and that treatment with the vitamin E significantly prevented the oxidative stress and lipid peroxidation.

Upregulation of microRNA-146a was not accompanied by downregulation of pro-inflammatory markers in diabetic kidney.

The present study was designed to evaluate whether microRNA-146a and its adapter proteins (TRAF6 and IRAK1) are involved in the pathogenesis of diabetes-induced kidney damage. Male Sprague-Dawley rats were divided into control and diabetic groups (n = 6 in each). Diabetes was induced by injection of streptozotocin (55 mg/kg; i.p.) in 12 h fasted rats. Diabetic kidney damage was diagnosed by renal hypertrophy, thickened glomerular basement membrane, widened filtration slits, mesangial expansion, as well as by elevated levels of blood urea and creatinine in diabetic rats 2 months after induction of diabetes. While the expression of NF-κB mRNA and miR-146a were increased in diabetic kidney compared to the sham controls (p < 0.01 for both comparisons), the mRNA levels of IRAK1 and TRAF6 did not statistically reduce. The NF-κB activity and the concentrations of TNF-α, IL-6 and IL-1ß in the kidney of diabetic rats were higher than the kidney of controls (p < 0.05 for TNF-α and NF-κB; p < 0.01 for IL-6 and IL-1ß). Our results indicate that the upregulation of miR-146a was not accompanied by downregulation of inflammatory mediators in diabetic kidney. It is possible that a defect in the miR-146a-mediated negative loop provides a situation for sustained activation of NF-κB and its targets to promote cells toward abnormalities.

Effects of quince leaf extract on biochemical markers and coronary histopathological changes in rabbits.

BACKGROUND: Atherosclerosis is the main cause of cardiovascular disease which is caused by a high-fat diet. Many of these patients use boiled quince leaves for their treatment. However, the supporting scientific information is limit. The aim of this study was to evaluate the effect of quince leaf on the progression of atherosclerosis and whether it can be an appropriate alternative to statins. METHODS: 24 male rabbits were randomly divided into two groups: normal diet (6 n) and high-cholesterol diet (2% cholesterol, 18 n) for 8 weeks. At the end of the 8 weeks, both groups underwent blood sampling and their biochemical markers were measured. Then, all animals in the normal-diet group and three of the high-cholesterol diet group were killed to investigate atheromic plaque in their coronary artery. The 15 remaining rabbits of the high-cholesterol diet group were randomly divided into 3 groups (5 n) after discontinuation of the fatty diet. The first group was not given any treatment, the second received atorvastatin (0.5 mg/kg) orally, and the third received quince leaf extract (50 mg/kg) orally for 12 weeks. At the end of this period, after blood sampling, biopsy of coronary artery was performed for histological study. RESULTS: The results showed that atorvastatin and quince leaf significantly decreased total cholesterol, triglyceride, LDL, AST, ALT, AP, BUN, and Cr levels compared with the first group of the high-cholesterol diet group (P < 0.05). No significant difference was found between atorvastatin and quince leaf extract groups in biochemical markers and atherosclerotic plaque in coronary artery. CONCLUSION: Atorvastatin and quince leaf extract can effectively prevent the progression of atherosclerosis in coronary arteries. According to the results of this study and also lower toxic effects of herbal medication compared to synthetic medication, leaf extract can be a substitute for statins in treatment and prevention of cardiovascular disease. The anti-atherosclerotic effect of quince leaf is most likely related to its antioxidant components.

Resveratrol improves diabetic retinopathy possibly through oxidative stress - nuclear factor κB - apoptosis pathway.

BACKGROUND: This study was designed to investigate the possible effectiveness of resveratrol (trans-3,5,4'-trihydroxystilbene) administration on oxidative stress, nuclear factor κB (NF-κB) activity and apoptosis rate in streptozotocin-nicotinamide-induced diabetic retinopathy. METHODS: Male Wistar rats were divided into four groups: normal control, diabetic control, normal rats treated with resveratrol, and diabetic rats treated with resveratrol. Diabetes was induced by injection of streptozotocin (50 mg/kg; ip), 15 min after the prescription of nicotinamide (110 mg/kg; ip) in 12 h fasted rats. RESULTS: Four-month oral resveratrol administration (5 mg/kg/day) significantly alleviated hyperglycemia, weight loss, enhancement of oxidative markers (lipid peroxidation index and oxidized to reduced glutathione ratio) and superoxide dismutase activity in both blood and retinas of the diabetic rats. Moreover, resveratrol administration to diabetic rats improved the elevated levels of retinas NF-κB activity and apoptosis rate. On the other hand, four months resveratrol administration prevented from disarrangement and reduction in thickness of retinal layers. CONCLUSION: These beneficial antidiabetic observations suggest that resveratrol may be considered as a therapeutic supplement to prevent from diabetic retinopathy.