Platelet rich plasma contains a collection of growth factors, and an optimal formulation, named O-rPRP, contains the highest possible concentration of growth factors. Purpose Challenging the healing power of O-rPRP in a high-galactose diet-induced premature ovarian insufficiency (POI) experimental rat model. Methods Rats were divided into four groups of ten rats each and treated for four week as follows; 1) the control group, fed with normal diet and received intraperitoneal (i.p.) injection of PBS once/week; 2) the POI group, fed with galactose diet (50%) and received PBS (i.p.) once/week; 3) the POI/O-rPRP group, fed a 50% galactose diet and received O-rPRP (i.p.) once/week; 4) the O-rPRP group (negative control), fed with a normal diet and received O-rPRP (i.p.) once/week. The levels of galactose, follicle stimulating hormone, 17 β-estradiol, anti-mullerian hormone and inhibin B were measured in serum samples. Western blotting and quantitative real-time PCR assays were employed to investigate the levels of miR-223, β1 integrin, p70S6k and MCL-1 in ovarian tissues. Results After O-rPRP treatment, β1 integrin expression was enhanced, and miR-223 expression was decreased. Unlike the untreated galactose group, in the group treated with O-rPRP, p70S6k and MCL-1 expression levels were increased, indicating that the mTOR growth signaling pathway was active and that apoptosis was inactive. After the introduction of O-rPRP, the number of follicles and the follicular maturation improved, which was consistent with the improvement of inhibin B levels and subsequent inhibition of FSH. Conclusion O-rPRP inhibited galactose-induced excessive atresia and provided an overall protective effect on the ovarian follicles.
Background:The possibility of exposure to a considerable amount of electromagnetic waves exists all around us. The hippocampus is involved in spatial memory and learning processes which could be compromised by exposure to cell phone emitted radiofrequency (RF)-electromagnetic field (EMF .( Objective: To explore the effect of exposure to EMF on hippocampal function and to throw more attention on the mechanisms of interaction in the form of hippocampal acetylcholine (ACh), glutamate, malondialdehyde (MDA) and hippocampal cellular responses mediated by autophagy (Atg7 gene expression) and mitochondrial repair mechanism (SIRT1( Subjects and Methods: This study was performed on 39 young apparently healthy male Wistar albino rats, initially weighing 70-90 grams. They were randomly divided into three equal groups: control group (group I), cell phone-EMF exposed group (group II), which was exposed to cell phone, 2 hours/day, 6 days/week for 12 weeks, and alpha lipoic acid-treated cell phone-exposed group (group III) which was exposed to EMF as group 2 and received i.p injection of alpha lipoic acid in a dose of 50 mg/kg for the last 3 weeks of cell phone exposure. Twelve weeks later, all rats were subjected to cognitive function test for learning and spatial memory using Morris water maze. Body weight changes and liver function tests (ALT and AST) were evaluated, then hippocampal levels of glutamate, ACh, MDA, gene expression of Atg7 and SIRT1 were measured.Results: Compared to the control rats, cell phone exposure in group II did not alter the cognitive function test and the hippocampal glutamate level, but it caused significant rise in hippocampal MDA and acetylcholine levels, though there was a higher non-significant increased expression of SIRT1 and Atg7. Lipoic acid treatment concomitant with EMF exposure induced increase in the time spent in target quadrant with shortened time to reach the platform on fifth day of training compared to the controls. Also, lipoic acidtreated cell phone exposed rats exhibited significantly enhanced hippocampal glutamate level accompanied by significantly reduced hippocampal MDA and acetylcholine levels compared to control rats and preserved higher but non-significant levels of SIRT1 and Atg7 expression. Conclusion:Increased hippocampal ACh and expression of SIRT1 and Atg7 could be the early protective response against the higher MDA with exposure, thereby preventing the negative impact of EMF exposure on learning and spatial memory. Lipoic acid treatment improved cognition by increasing glutamate necessary for long term potentiation and decreasing hippocampal MDA.
Background: Lead contamination has turned into a major concern as it serves no useful purpose in the human body. Its presence in the body can lead to toxic effects on different organs. Aim:The purpose of the present study is to examine the efficacy of selenium in mitigating leadinduced oxidative stress and kidney injury in male albino Wistar rats. Further to study the underlying molecular mechanism. Methods: We hypothesized that selenium protect against lead nephrotoxicity by testing various parameters of kidney function in male rats treated for 28 days with o.5 mg/kg selenium versus control male rats that received a vehicle. Results: The results showed an increase of serum urea, creatinine, uric acid and urinary albumin in rats intoxicated with lead compared to control group. The increase of these parameters would indicate renal toxicity which is confirmed by histopathological changes. Lead intoxicated rats had significant increment in apoptosis as well as phosphorylated PERK, eIF2α and apoptotic proteins as CHOP, caspase 3 and 8 in the kidneys, which were attenuated by selenium treatment. Conclusion: This study clearly demonstrated that activation of PERK-eIF2α -CHOP signaling pathway was involved in lead induced nephrotoxicity in rats and selenium inhibited lead nephrotoxicity partly through suppression of PERK-eIF2α CHOP pathway.
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