Search

Introduction: Musculoskeletal injuries are widespread causes of sport injuries. Ordinary therapy is inadequate for rapid healing. So, in this study, the therapeutic effects of platelet rich plasma (PRP) were investigated as it is simple, efficient, and minimally invasive, and lessen recovery time. Materials and Methods: Fifty-four adult male albino rats, were categorizes into four groups: Group I (control group). Group II had a crush injury to the right gastrocnemius muscle, then sacrificed after 2 hours. Group III received no treatment and were subdivided into subgroups III A and III B, each includes 6 rats sacrificed after 7 and 14 days, respectively. Group IV, were injected immediately after injury by 0.1 ml PRP in injury site, then were subdivided into subgroups IV A and IV B, each includes 6 rats sacrificed after 7 and 14 days, respectively. Blood samples were analyzed for serum creatine phosphokinase (CPK) level. Sections from the middle part of the right gastrocnemius muscle were processed for histological assessment using H. and E., Masson trichrome stain, immunohistochemical staining for myogenin immunoreactivity, in addition to semithin and ultra-thin sections for light and electron microscopic examination, followed by morphometric and statistical studies. Results: Sections of group II showed disorganized, fragmented, discontinued, and tapering muscle fibers, disrupted Z discs at focal areas and giant disfigured mitochondria. The CPK level and mean number of myogenin immunoreactive nuclei and mean area percent of fibrous tissue were elevated, while the mean diameter of muscle fibers was decreased versus the control. Group III showed partial improvement, significant decrease in CPK level and increase in mean area percent of fibrous tissue, mean number of myogenin immunoreactive nuclei and in fiber diameter. Group IV showed prominent improvement. Conclusion: Platelet rich plasma could enhance repair of acutely crushed skeletal muscle and accelerate the healing process with minimal fibrosis. [ABSTRACT FROM AUTHOR]

Background: Myocardial infarction (MI) is a leading cause of morbidity and mortality. It is associated with oxidative stress, apoptosis and inflammation. Zinc (Zn) and vitamin E (VE) are known to exert antioxidant and anti-inflammatory effects. Aim of the Work: Evaluate the cardioprotective potential of Zn, VE and their combination against isoprenaline (ISO)- induced myocardial infarction in adult male albino rats. Materials and Methods: Forty rats divided into five groups; I (control), II (ISO group): rats were injected subcutaneously (SC) with ISO (100 mg/kg) on the 20th and 21st days at interval of 24 h. Groups III (Zn group), IV (VE group) and V (ZE group): rats received respectively daily Zn (30 mg/kg), VE (100 mg/kg) or combination of both orally for 21 days and injected with ISO as group II. On the 22nd day, electrocardiography, biochemical and histological studies were done. Myocardial sections were subjected to H&E, caspase-3 and beclin 1 immunohistochemical stains. This was followed by morphometric and statistical analysis. Results: Group II exhibited significant electrocardiographic and biochemical changes compared to the control; deterioration of cardiac function with elevated cardiac enzymes, MDA, TNF-α and mTOR, in addition to reduced SOD, IL-10 and AMPK. Myocardial sections showed disturbed architecture with marked inflammatory infiltration and significantly increased caspase-3 and decreased beclin 1 immunoexpression. Groups III and IV revealed decreased cardiac enzymes, MDA, TNF-α and mTOR, in addition to elevated SOD, IL-10 and AMPK. Myocardial sections showed nearly normal histology with significantly decreased caspase-3 and increased beclin 1 immunoexpression. Group V presented the most protection with results significant to both groups III and IV. Conclusion: Combined Zn and VE pretreatment proved to have protective effect against ISO-induced MI more than using either of them alone regarding the electrocardiography, biochemical and histological parameters and this was through targeting autophagy and modulating its AMPK-mTOR pathway. [ABSTRACT FROM AUTHOR]

Background: Diabetic neuropathy (DN) is a major chronic diabetes complication characterized by functional and structural alterations in peripheral nerves. Platelet rich plasma (PRP) is an encouraged biological blood derivative that has gained publicity in diverse applications and proved its efficacy. Aim of Work: Evaluate the probable ameliorating effect of platelet poor plasma (PPP) versus PRP on induced DN in rats. Materials and Methods: This study included 48 male adult albino rats, 10 to obtain PRP and PPP. Thirty eight were divided into 4 groups; group I (control). Group II (DN group): received a single intraperitoneal STZ (60 mg/kg) injection and were left till the end of the experiment. Groups III (PRP group) and IV (PPP group) received subcutaneous PRP or PPP 0.5 mL/kg, 2 times a week for 3 weeks after 60 days diabetes. Body weight, blood glucose and miR-146a and nerve conduction velocity (NCV) were assessed, as well as tissue MDA, TNFα, NGF, ZO-1 and claudin-1. Right sciatic nerve specimens were taken and processed for HandE, toluidine blue stains, S100, CD34 and caspase-3 immunohistochemical stains and TEM. Number of CD34 immunopositive cells and area percent of S100 and caspase-3 immunoreaction were measured, in addition to G-ratio and capillary luminal area. This was followed by statistical analysis. Results: DN group showed altered biochemical and histological features; axonopathy, Schwannopathy and angiopathy, with affected NCV and telocyte-like cells (TLCs). PRP and PPP groups showed comparable results to each other and to the control. They revealed almost normal biochemical and histological features and NCV. In addition, they revealed significant increase in S100 and CD34 immunoexpression with significant decrease in area percent of caspase-3 versus DN group. Conclusion: PPP and PRP proved to exert ameliorative effect on DN through improving the biochemical and histopathological altera¬tions and TLCs preservation. [ABSTRACT FROM AUTHOR]

Introduction: Ulcerative colitis (UC) is a chronic inflammatory condition characterized by acute episodes of colonic inflammation. Its pathogenesis is associated with decreased antioxidant capability. Royal Jelly (RJ) is usually used as a complementary therapy in various diseases because of its antioxidant, anti-inflammatory and immunomodulatory effects. Aim of the work: To evaluate the protective effect of RJ against acetic acid-induced UC in adult male albino rats. Materials and Methods: Thirty rats were divided equally into 3 groups. Group I was the control group. Group II included rats subjected to intracolonic acetic acid (AA) for induction of UC. Group III 10 rats treated with RJ (250 mg/kg/day orally) for 7 days, thereafter subjected to AA. RJ was administered for another 14 days. Rats were sacrificed after 21 days. Serum glutathione (GSH) and malondialdehyde (MDA) were assessed. Colonic sections were subjected to H&E, Periodic Acid Schiff (PAS), toluidine blue, Mallory's trichrome stains and cyclooxygenase-2 (COX-2) immunohistochemical stain. Results: Group II showed significant decrease in GSH, significant increase in MDA and marked histological alterations in colon. There was a significant decrease in the number of goblet cells, but significant increases in the number of mast cells, area% of collagen fibers and COX-2 immunoexpression compared to the control. In group III, GSH was significantly increased and MDA was significantly decreased compared to group II. The colon showed minimal changes, significant increase in the number of goblet cells, significant reduction in the number of mast cells, collagen deposition and COX-2 immunoreactivity compared to group II. When compared to the control, there was no significant difference regards the serological, histological and morphometric results, except for the number of goblet cells that revealed significant decrease. Conclusion: RJ proven to protect against acetic acid-induced UC in albino rats. [ABSTRACT FROM AUTHOR]

Introduction: Hyperprolactinemia (HPRL) commonly causes primary amenorrhea and reproductive disorders. Resveratrol (RES), a natural phenol, possesses antioxidant, anti-inflammatory and anti-apoptotic effects. However, its protective role on the histological structure of female reproductive organs in case of HPRL remains unclear. Aim of the work: This study aimed at evaluating the protective effect of RES against the HPRL induced by metoclopramide in female albino rats. Materials and Methods: Female rats that showed three regular estrus cycles (determined by vaginal smears) were divided into three groups. Group I was the control group. Group II rats were given oral metoclopramide (2 mg/Kg/day) for 28 consecutive days. Group III rats were given oral RES (20 mg/kg/day) for 28 days concurrently with metoclopramide. Serum superoxide anion (O2-), prolactin (PRL), estradiol (E2), progesterone, follicle stimulating hormone (FSH) and luteinizing hormone (LH) were assessed, in addition to measurement of tissues tumor necrosis factor-alpha (TNF-α). Sections from uteri, oviducts and ovaries were stained with hematoxylin and eosin and caspase-3 immunohistochemical stain and were subjected to morphometric and statistical studies. Results: Group II showed significant increase in O2-, TNF-α and PRL, with significant decrease in the sex hormones. There were histological alterations in the uteri, oviducts and ovaries, with significant increased caspase-3 immunoexpression compared to the control. While, in group III, there was significant decrease in O2-, TNF-α and PRL, with significant increase in the sex hormones. The uteri, oviducts and ovaries showed minimal changes, with significant reduction in caspase-3 immunoreactivity compared to group II. Conclusion: Administration of resveratrol ameliorates the oxidative stress, inflammation, hormonal assay alterations, histological changes and apoptosis resulted from induced HPRL in female rats. [ABSTRACT FROM AUTHOR]

Background: Testicular damage is one of the most hazardous effects of chemotherapy as it is frequently associated with oligozoospermia and azoospermia., Aim of the Work: This study aimed at evaluating the protective effect of hematopoietic stem cell mobilization by granulocyte colony-stimulating factor (G-CSF) in a rat model of busulfan-induced testicular injury., Materials and Methods: Twenty-four adult albino rats were divided into four groups: group I, the control, Group II: rats received two doses of busulfan (each 15 mg/kg) intraperitoneally (IP) with 14 days interval, Group III: rats received busulfan and left untreated, and Group IV received busulfan IP then G-CSF (70 μg/kg/day) subcutaneously for 5 consecutive days. Testicular sections were stained with H and E and immunohistochemically for CD34, proliferating cell nuclear antigen (PCNA) and caspase-3, and semithin sections were stained with toluidine blue., Results: Groups II and III showed loss of the normal histological architecture of the testis and spermatogenic cells, with increased apoptosis confirmed by significantly increased caspase-3 and significantly decreased PCNA immunoexpression. While Group IV revealed improved testicular histology, decreased apoptosis, and increased proliferative capacity of spermatogenic cells. This was confirmed by significantly decreased caspase-3 immunoexpression and increased PCNA immunoreaction., Conclusion: Mobilization of stem cells with G-CSF was found to improve the testicular histology following busulfan chemotherapy in albino rats., Competing Interests: There are no conflicts of interest.