Background: Determination of postmortem interval (PMI) has always been a fundamental issue in forensic fields. Therefore, the purpose of this study was to assess usefulness of histopathological changes and collagen degradation in the prostate for estimation of PMI in adult male rats. Methods: Forty male albino rats were euthanized using CO2 chamber and then classified randomly into 8 groups; each group consisted of 5 rats. Rats were used for determining postmortem changes at 0, 6, 12, 24, 36, 48, 60 and 72 hs. Sections of prostate were fixed and stained for histopathology and quantitative analysis of collagen by Masson trichrome. Moreover, slices of 5µm mounted on positively charged slides were carried out for collagen III immunohistochemistry. Results: The prostate showed normal histology at 0 and 6 hs postmortem (PM). While, at 12 hs, most sections of the gland revealed no abnormalities except for mild focal widening between the acini. Starting from 24 hs, epithelial desquamation was seen in most acini. Seventy-two hours, obvious necrosis of prostatic acini appeared in most of samples. Degradation of collagen started and the spaces between acini became wide at 12 and 24 hs PM. Complete loss of stain reactivity was observed at both 60 and 72 hs. Moreover, a significant decrease in the amount of collagen's stained areas in the prostate started from 12 hs. Positive immunohistochemical reaction of collagen III was detected at 0, 6 and 12 hs PM. However, it was completely lost at 60 and 72 hs. Interestingly, the immuno-reactive area of collagen III was significantly increased at 6 hs, then a remarkable decline in immuno-reactive area was observed at 12 hs. Conclusion: Collagen type III proved to be a successful parameter with histopathology in determination of PM interval. However, further studies still needed to confirm the accuracy of these parameters.
Angiogenesis accelerates tissue regeneration in a variety of ischemic conditions including myocardial infarction (MI) and constitutes a valuable approach for post‐MI repair. Here we investigated whether angiogenesis promotion induced by α7‐nicotinic acetylcholine receptors (α7‐nAChRs) mitigates histopathological, electrocardiographic, and molecular consequences of MI in rats. These profiles were evaluated in rats with isoprenaline (85 mg/kg/day i.p. for 2 days)‐induced MI and co‐treated subcutaneously with nicotine (20 μg/kg/day s.c.), PHA‐543613 (PHA, selective α7‐nAChR agonist, 20 μg/kg/day), methyllycaconitine (MLA, selective α7‐nAChR antagonist, 40 μg/kg/day) plus nicotine, or the vehicle for 16 consecutive days. Isoprenaline‐insulted rats showed (i) ECG signs of MI such as significant ST‐segment elevations and prolonged QT‐intervals, (ii) deteriorated left ventricular histopathological scoring and elevated inflammatory cell infiltration, (iii) reduced immunohistochemical expression of cardiac CD34, a biomarker of capillary density, (iv) decreased cardiac expression of iNOS and α7‐nAChRs, and (v) adaptive increases in cardiac HO‐1 expression and plasma angiogenic markers such as vascular endothelial growth factor (VEGF) and nitric oxide (NO). These effects of isoprenaline, except cardiac iNOS and α7‐nAChRs downregulation, were ameliorated in rats co‐treated with nicotine or the selective α7‐nAChR agonist PHA for 16 consecutive days. We also show that concurrent α7‐nAChR blockade by MLA reversed the ECG, histopathological, and capillary density effects of nicotine, thereby reinforcing the advantageous cardioprotective and anti‐ischemic roles of α7‐nAChRs in this setting. In conclusion, the activation of α7‐nAChRs with PHA or doses of nicotine in the microgram scale promotes neovascularization and offers a promising therapeutic strategy for MI.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Background: Bisphenol A (BPA) is a widely used and environmentally spread plasticizer. BPA has various toxic effects, including immunological alterations. Aim: Current work aimed to investigate the effect of BPA and protection with lycopene (LYC) on immunological parameters. Material and Methods: Twenty-four male albino were divided into 4 equal groups. Control group received corn oil, LYC group was given LYC 5 mg/kg, BPA group was given BPA at 5 mg/kg. Last group was given combination of BPA and LYC the same previous doses. Treatments were given daily via oral gavage for 4 weeks. Weight gain, food conversion ratio (FCR), hematological parameters and lymphocytes proliferation assay were determined. Serum total antioxidant capacity (TAC), malondialdehyde (MDA), interleukin-1β (IL-1β), Interleukin-12 (IL-12) and lymphocytes comet assay were evaluated. Spleen and thymus histopathological assessment was done. Results: BPA significantly (P<0.05) increased FCR while decreased lymphocytes proliferation than control group however, hematological parameters didn't alter. Serum TAC was significantly (P<0.05) reduced in BPA group than control group while MDA, IL-1β and IL-12 were significantly (p<0.05) increased than control group. Lymphocyte showed significant increase in comet tail and % of damage. Thymus and spleen revealed mild lymphoid depletion. Conclusion: BPA induced immunological perturbations that favors pro-inflammation and autoimmunity. LYC administration ameliorated oxidative stress and lipid peroxidation induced immunological disorders.
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