Delivery by cesarean section leads to heavier adult bodyweight in prairie voles (Microtus ochrogaster).

Delivery by cesarean section now makes up 32.1 % of all births in the United States. Meta-analyses have estimated that delivery by cesarean section is associated with a > 50 % increased risk for childhood obesity by 5 years of age. While this association is independent of maternal obesity, breastfeeding, and heritable factors, studies in humans have been unable to test for a causal role of cesarean delivery in this regard. Here, we set out to use an animal model to experimentally test whether delivery by cesarean section would increase offspring weight in adulthood. Delivery by cesarean section may exert neurodevelopmental consequences by impacting hormones that are important at birth as well as during metabolic regulation in later life, such as oxytocin and vasopressin. The prairie vole (Microtus ochrogaster) has long been studied to investigate the roles of oxytocin and vasopressin in brain development and social behavior. Here, we establish that prairie voles tolerate a range of ambient temperatures, including conventional 22° housing, which makes them translationally appropriate for studies of diet-induced obesity. We also studied vole offspring for their growth, sucrose preference, home cage locomotor activity, and food consumption after birth by either cesarean section or vaginal delivery. At sacrifice, we collected measures of weight, length, and adipose tissue to analyze body composition in adulthood. Voles delivered by cesarean section had consistently greater bodyweights than those born vaginally, despite having lower food consumption and greater locomotive activity. Cesarean-delivered animals were also longer, though this did not explain their greater body weights. While cesarean delivery had no effect on vasopressin, it resulted in less oxytocin immunoreactivity within the hypothalamus in adulthood. These results support the case that cesarean section delivery plays a causal role in increasing offspring body weight, potentially by affecting the oxytocin system.

Curcumin protects against lamotrigine-induced chronic ovarian and uterine toxicity in rats by regulating PPAR-γ and ROS production.

Lamotrigine (LTG) is an antiepileptic drug with possible adverse effects on the female reproductive system. Curcumin was declared to improve ovarian performance. Therefore, this study aimed to clarify ovulatory dysfunction (OD) associated with LTG and the role of curcumin in ameliorating this dysfunction. Adult female Wister albino rats were assigned into four groups: negative control (received saline), positive control (received curcumin only), LTG, and LTG with curcumin groups. Drugs were administered for 90 days. The hormonal profile, including testosterone, estrogen, progesterone, luteinizing hormone, and follicle-stimulating hormone, in addition to the lipid profile and glycemic analysis, were tested. Oxidative stress biomarkers analysis in the ovaries and uterus and peroxisome proliferator-activated receptor-γ (PPAR-γ) gene expression were also included. Histopathological examination of ovarian and uterine tissues and immunohistochemical studies were also performed. Curcumin could improve the OD related to chronic LTG intake. That was proved by the normalization of the hormonal profile, glycemic control, lipidemic status, oxidative stress markers, and PPAR-γ gene expression. The histopathological and immunohistochemical examination of ovarian and uterine tissues revealed an improvement after curcumin administration. The results describe an obvious deterioration in ovarian performance with LTG through the effect on lipidemic status, PPAR-γ gene, and creating an oxidative stress condition in the ovaries of chronic users, with a prominent improvement with curcumin addition to the treatment protocol.

Protective effect of rivastigmine against lung injury in acute pancreatitis model in rats via Hsp 70/IL6/ NF-κB signaling cascade.

Acute lung injury (ALI) that develops as a result of AP can progress to acute respiratory distress syndrome. Some hypotheses are proposed to explain the pathophysiology of AP and its related pulmonary hazards. This experiment aimed to evaluate the mitigating action of rivastigmine (Riva) in lung injury that occurs on the top of acute pancreatitis (AP) induced in rats. Thirty-two male Wister rats were randomized to one of four groups: control, Riva-treated, acute pancreatitis (AP), and acute pancreatitis treated by Riva. Serum amylase and lipase levels were assessed. Pulmonary oxidative stress and inflammatory indicators were estimated. A pancreatic and pulmonary histopathological examination, as well as an immunohistochemical study of HSP70, was carried out. Riva significantly attenuated the L-arginine-related lung injury that was characterized by increased pulmonary inflammatory biomarkers (interleukin-6 [IL-6]), nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), increased pulmonary oxidative markers (total nitrite/nitrate [NOx]), MDA, decreased total antioxidant capacity (TAC), and reduced glutathione level (GSH)) with increased caspase-3 expression. Therefore, Riva retains potent ameliorative effects against lung injury that occur on the top of AP by relieving oxidative stress, inflammation, and apoptosis via HSP70/IL6/NF-κB signaling.

Dipeptidyl peptidase-4 inhibitor: Sitagliptin down-regulated toll-like receptor 4 signaling pathway to reduce uterine injury in rats.

Objectives: Uterine ischemia is a common problem with ongoing controversy about its pathogenesis and prevention. The present study aimed to investigate the protective role of sitagliptin against uterine ischemia-reperfusion injury (IRI). Materials and Methods: Rats were allocated into 4 groups: control, sitagliptin (SIT) (5 mg/kg), IR; ischemia was induced followed by reperfusion, and IR+SIT; SIT was administered 1 hr before IRI. Uteri were removed for histopathological and biochemical observations. Malondialdehyde (MDA), total nitrites (NOx), reduced glutathione (GSH), superoxide dismutase (SOD) activity, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and toll-like receptor 4 (TLR4) were all measured. Hematoxylin and eosin (H&E) stain, Periodic acid-Schiff stain (PAS), and caspase-3 immunostaining were applied. Results: In the IR+SIT group; NOx, GSH, and SOD activities increased significantly. Meanwhile, the levels of MDA, TNF-α, IL-6, TLR4, and caspase-3 immunoexpression showed a significant reduction, as compared with the IR group. In the IR+SIT group, an improvement in the histopathological picture was noticed. Conclusion: The results showed that sitagliptin confers protection against uterine IRI through anti-oxidant, anti-inflammatory, and anti-apoptotic effects with a possible role for TLR4.

Rivastigmine ameliorates indomethacin experimentally induced gastric mucosal injury via activating α7nAChR with inhibiting oxidative stress and apoptosis.

The current study aimed to investigate the potential ameliorative role of Rivastigmine (RIVA), the anti-Alzheimer drug, against the gastric mucosal injury caused by indomethacin (IND). The rats were divided into four groups: group I was given a vehicle as a control, group II was given RIVA (0.3 mg/kg) once daily intraperitoneal (ip) for 2 weeks, group III was given a single IP dose of 30 mg/kg IND, and group IV was given RIVA ip 2 weeks before the administration of IND. The gastric mucosal injury was detected by the estimation of ulcer index, gastric acidity, pepsin, and mucin concentrations. Malondialdehyde (MDA), superoxide dismutase (SOD), reduced glutathione (GSH), total nitrite/nitrate (NOx), and the expression of tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), nuclear factor kappa B (NF-κB), Hemoxygenase 1 (HO-1), and caspase-3 were all measured in gastric tissue. In addition, histological assessment and proliferating cell nuclear antigen (PCNA) immuno-expression were studied. Gastric mucosal injury induced by IND was indicated by both biochemical and histopathological assessments. RIVA Pretreatment reduced ulcer index, MDA, TNF-α, IL-6, NF-κB, and caspase-3 and increased SOD, GSH, NOx, and HO-1. RIVA improved the suppressed nuclear immunoreaction for PCNA observed with IND. The current findings provide novel evidence that RIVA possesses a prophylactic action against IND-induced gastric mucosal damage in rats. Despite being a cholinergic drug that is associated with increased pepsin and stomach acidity, RIVA protected against IND-induced gastric mucosal injury via activating α7nAChR and inhibiting oxidative stress and apoptosis.

Xanthine Oxidase Inhibitor, Febuxostat Is Effective against 5-Fluorouracil-Induced Parotid Salivary Gland Injury in Rats Via Inhibition of Oxidative Stress, Inflammation and Targeting TRPC1/CHOP Signalling Pathway.

The current research aimed to examine the ameliorative role of febuxostat (FEB), a highly potent xanthine oxidase inhibitor, against 5-fluorouracil (5-FU)-induced parotid salivary gland damage in rats, as FEB is a pleiotropic drug that has multiple pharmacological effects. A total of 32 Wistar adult male rats were randomly arranged into four groups. Group 1: the control group; given only the vehicle for 14 days, then given a saline i.p. injection from the 10th to the 14th day. Group 2: the FEB group; rats received FEB (10 mg/kg) once daily po for 14 days before receiving a saline i.p. injection from the 10th to the 14th day. Group 3: the 5-FU group; from the 10th to the 14th day, rats received an intraperitoneal injection of 5-FU (35 mg/kg/day). Group 4: the FEB/5-FU group; rats were pre-treated with FEB po for 14 days before receiving 5-FU i.p injections for five consecutive days from the 10th to the 14th day. Parotid gland damage was detected histologically and biochemically by the evaluation of oxidative stress markers (malondialdehyde (MDA) and nitric oxide levels (NOx)), oxidant defences (reduced glutathione (GSH) and superoxide dismutase (SOD)), inflammatory markers (tumour necrosis factor-alpha (TNF-α), interleukin-1ß (IL-1ß)), and transient receptor potential canonical1 (TRCP1) and C/EBP homologous protein (CHOP). FEB pre-treatment reduced MDA, TNF-, and IL-1 while increasing SOD, GSH, and NOx. FEB also significantly increased TRPC1 and decreased CHOP in parotid gland tissue. In conclusion, FEB pre-treatment reduced 5-FU-induced parotid salivary gland damage not only through its powerful anti-inflammatory and antioxidant effects, but also through its effect on the TRPC1/CHOP signalling pathway.

Role of IL-6/STAT3 pathway in mediating the protective effect of agomelatine against methotrexate-induced lung/intestinal tissues damage in rats.

BACKGROUND: Methotrexate (MTX), an anticancer drug, has been linked to multiple organ toxicity. The drug-induced acute toxic symptoms can negatively affect the patient's commitment to the course of treatment. MATERIALS AND METHODS: This study aimed to investigate the mitigating action of agomelatine (Ago) against MTX-induced lung and intestinal toxicity. Forty eight male Wister rats were randomized into six experimental groups: Group 1: Control; Groups 2 and 3: received Ago L&H (20/40 mg/kg, respectively by gavage); Group 4: received MTX 10 mg/kg/day, i.p. on days 7-9; Group 5: received Ago L (20 mg/kg) + MTX; Group 6: received Ago H (40 mg/kg) +MTX. The duration of the study was 10 days. Lung/intestine oxidative markers were measured. Lung/intestinal tissues IL-6, STAT3, and HO-1 levels were evaluated by ELISA. Besides, lung/intestinal tissues were examined for Histological changes, collagen fibers detection using Massonꞌs trichome stain, and immunohistochemical study using HSP70 antibody. RESULTS: MDA, NOx, IL-6, and STAT3 levels were significantly higher in the MTX group's lungs and intestines, indicating lung and intestinal toxicity. There were substantial decreases in GSH, SOD tissue levels, and HSP 70 immunoexpression, as well as histological changes suggesting significant lung and intestinal injury. All of the above parameters improved significantly by using Ago. CONCLUSION: By reducing oxidative stress, inflammatory processes, and modulating the IL-6/STAT3 pathway, Ago has potent ameliorative effects against MTX-induced lung/intestinal toxicities.

Dapsone Ameliorates Isoproterenol-Induced Myocardial Infarction via Nrf2/ HO-1; TLR4/ TNF-α Signaling Pathways and the Suppression of Oxidative Stress, Inflammation, and Apoptosis in Rats.

Myocardial infarction (MI) is a critical condition that can happen with high doses or rapid termination of beta blockers therapy. The study aimed to evaluate the potential anti-toxic value of DAP against isoproterenol (ISO) - induced MI. Twenty-eight male Wistar rats were used for the study. The rodents were assigned to four groups (n = 7) and the treatments were given for 12 days as follows; Group 1 (control): were administrated normal saline, Group 2 (DAP control): were administrated DAP (10 mg/kg/day IP), Group 3 (ISO group): were administrated ISO (100 mg/kg, IP on the 11th and 12th days of the experiment), and Group 4 (DAP + ISO): co-treated with DAP plus ISO. The measured parameters were cardiac malondialdehyde (MDA), reduced glutathione (GSH), total nitrite/nitrate (NOx), catalase (CAT), serum cardiac biomarkers; CK-MB, ALT, LDH, and ALK-PH. Also, interleukin-1ß (IL-1ß), tumor necrosis factor-alpha (TNF-α), Nuclear factor (erythroid-derived 2)-like 2 (Nrf2), heme oxygenase-1 (HO-1), toll-like receptor 4 (TLR4), caspase-3 activity, and hepatic BAX and Bcl-2 were also assessed. Also, histological examination and vimentin immuno-expressions were studied. ISO group exhibited MI as evidenced by the elevation in serum cardiac biomarkers, MDA, NOx, IL-1ß, TNF-α, and caspase-3 together with the reduction in GSH, Nrf2, HO-1 levels, and a faint vimentin immuno-reaction. Histological alterations revealing distorted cardiomyocytes; vacuolation, edema, pyknosis, and fragmentation were also noticed. DAP significantly ameliorated all the examined toxicity indicators. DAP revealed efficient ameliorative actions against ISO-caused MI by marked reduction in myocardial infarct size and suppressed oxidative stress, inflammation, and apoptosis via the up-regulation of the Nrf2/HO-1; TLR4/TNF-α signaling pathways.

Clinical characteristics and outcomes in women and men hospitalized for coronavirus disease 2019 in New Orleans.

OBJECTIVES: Determine if sex differences exist in clinical characteristics and outcomes of adults hospitalized for coronavirus disease 2019 (COVID-19) in a US healthcare system. DESIGN: Case series study. SETTING AND PARTICIPANTS: Sequentially hospitalized adults admitted for COVID-19 at two tertiary care academic hospitals in New Orleans, LA, between 27 February and 15 July 2020. MEASURES AND OUTCOMES: Measures included demographics, comorbidities, presenting symptoms, and laboratory results. Outcomes included intensive care unit admission (ICU), invasive mechanical ventilation (IMV), and in-hospital death. RESULTS: We included 776 patients (median age 60.5 years; 61.4% women, 75% non-Hispanic Black). Rates of ICU, IMV, and death were similar in both sexes. In women versus men, obesity (63.8 vs 41.6%, P < 0.0001), hypertension (77.6 vs 70.1%, P = 0.02), diabetes (38.2 vs 31.8%, P = 0.06), chronic obstructive pulmonary disease (COPD, 22.1 vs 15.1%, P = 0.015), and asthma (14.3 vs 6.9%, P = 0.001) were more prevalent. More women exhibited dyspnea (61.2 vs 53.7%, P = 0.04), fatigue (35.7 vs 28.5%, P = 0.03), and digestive symptoms (39.3 vs 32.8%, P = 0.06) than men. Obesity was associated with IMV at a lower BMI (> 35) in women, but the magnitude of the effect of morbid obesity (BMI ≥ 40) was similar in both sexes. COPD was associated with ICU (adjusted OR (aOR), 2.6; 95%CI, 1.5-4.3) and IMV (aOR, 1.8; 95%CI, 1.2-3.1) in women only. Diabetes (aOR, 2.6; 95%CI, 1.2-2.9), chronic kidney disease (aOR, 2.2; 95%CI, 1.3-5.2), elevated neutrophil-to-lymphocyte ratio (aOR, 2.5; 95%CI, 1.4-4.3), and elevated ferritin (aOR, 3.6; 95%CI, 1.7-7.3) were independent predictors of death in women only. In contrast, elevated D-dimer was an independent predictor of ICU (aOR, 7.3; 95%CI, 2.7-19.5), IMV (aOR, 6.5; 95%CI, 2.1-20.4), and death (aOR, 4.5; 95%CI, 1.2-16.4) in men only. CONCLUSIONS: This study highlights sex disparities in clinical determinants of severe outcomes in COVID-19 patients that may inform management and prevention strategies to ensure gender equity.

Vitamin E protects against gabapentin-induced chronic hepatic and renal damage associated with the inhibition of apoptosis and tissue injury in rats.

AIMS: This study aimed to investigate the potential protective effects of vitamin E against gabapentin-induced chronic liver and kidney injury associated with the inhibition of biomarkers of apoptosis and tissue injury. MATERIALS AND METHODS: Four groups of adult male rats were included; control, gabapentin (100 mg/kg/day), Vitamin E (80 mg/kg/day), and a combination of gabapentin and Vitamin E for 90 days. Serum levels of AST, ALT, LDH, ALP, urea, and creatinine were measured in addition to malondialdehyde (MDA), and reduced glutathione (GSH) tissue levels. P53 gene expression, histological, and immunohistochemical examinations were performed in liver and kidney tissue samples. KEY FINDINGS: Gabapentin increased AST, ALT, LDH, ALP, urea, creatinine, MDA, and p53 gene expression and it reduced GSH. Moreover, gabapentin administration caused structural changes in the hepatic and renal architecture with a weak Periodic acid-Schiff (PAS) reaction that reflects glycogen deposition in the liver and kidney and a positive immunoreaction for BCL2-associated X protein (BAX) that reflects activated apoptosis. Vitamin E significantly (p<0.05) reversed the biochemical alterations associated with chronic gabapentin administration and improved the histopathological picture of hepatic and renal tissue with a partial inhibition of BAX. SIGNIFICANCE: Chronic administration of gabapentin causes hepatic and renal impairments, which is ameliorated by Vitamin E; possibly due to the inhibition of biomarkers of apoptosis and tissue injury.

Evaluation of time passed since death by examination of oxidative stress markers, histopathological, and molecular changes of major organs in male albino rats.

Recent biochemical, metabolic, and molecular profiles of various body fluids showed more accurate correlation to the postmortem interval than the traditional physical examination. Our study aimed to evaluate time passed since death in relation to oxidative stress markers, HMGB1 genetic expression, histopathological examination, and BCL2 immunohistochemical analysis in major organs (heart, kidney, and testis). Forty-two adult male rats were included and randomly divided into seven equal groups. After sacrification, the rodents were kept at room temperature and major organs were obtained at 0, 12, 24, 48, 72, 96, and 120 h. Malonaldehyde (MDA), superoxide dismutase (SOD), reduced glutathione (GSH) tissue levels, High mobility group box 1 protein (HMGB1) gene expression, histopathological, and B cell lymphoma 2 (BCL2) immunohistochemical expressions were analyzed. Postmortem interval was correlated to different tissue levels of MDA, SOD, and GSH. HMGB1 showed enhanced postmortem gene expression with a peak at 48 h after death. Obvious time-dependent histopathological changes were observed in all the examined organs. Dilated spaces, extravasation, and fragmentation scores in heart specimens were higher at 96 and 120 h compared with the other groups. Renal changes in the form of shrunken glomeruli, loss of tubular epithelium, and hyalinization and testicular findings in the form of epithelial detachment, vacuolation, and loss of sperms started at 72 h postmortem. BCL2 expression began to decrease 24 h and became negative at 96 h after death. In conclusion, HMGB1 gene expression can be used for estimation of time passed since death as it shows time-dependent changes in the form of a progressive increase with a peak at 48 h then it begins to decline. Oxidants and antioxidants are correlated to PMI until 120 h after death. Histopathological changes in the heart, kidney, and testis are also time-dependent until the 5th day after death. BCL2 immunohistochemical expression begins to decline 24 h until 96 h after death when it becomes negative.

Vinpocetine ameliorates L-arginine induced acute pancreatitis via Sirt1/Nrf2/TNF pathway and inhibition of oxidative stress, inflammation, and apoptosis.

OBJECTIVES: Acute pancreatitis (AP) is a common severe critical illness with a high mortality rate. We aimed to study the effect of vinpocetine (Vinpo) in the treatment of AP because of its anti-inflammatory, antioxidant, and antiapoptotic effects. MATERIALS AND METHODS: Thirty two adult male albino Wistar rats were randomized to four groups: control group, Vinpo group (20 mg/kg.P.O.), l-arginine group (two intraperitoneal injections of l-arginine 2.5 g/kg, 1 h apart), and Vinpo + L-arginine group. Vinpo administration was once daily for 7 consecutive days and started 1 h later after l-arginine administration. We measured serum enzyme biomarkers (lipase and amylase), levels of pancreatic malondialdehyde (MDA), total antioxidant capacity (TAC), reduced glutathione (GSH), total sulfhydryl (T-SH), total nitrite/nitrate (NOx), Interluken-6 (IL-6), tumor necrosis factor-alpha (TNF-α), Nuclear factor (erythroid-derived 2)-like 2 (Nrf2), Sirtuin type 1 (Sirt1), and caspase-3 activity. Furthermore; histological changes, anti-insulin, and inducible nitric oxide synthase (iNOS) immuno-expressions were examined. RESULTS: l-arginine group displayed AP as manifested by a significant increase in serum lipase and amylase, MDA, NOx, IL-6, TNF-α, caspase-3 with iNOS immuno-expression. Histological changes indicating marked pancreatic injury were observed together with a significant decrease in TAC, GSH, T-SH, Nrf2, Sirt1 levels, and anti-insulin immuno-expression. Vinpo showed a significant amelioration in all parameters. CONCLUSION: Vinpo possesses potent ameliorative effects against AP by decreasing oxidative stress, inflammatory process, and apoptosis through regulation of the Sirt1/Nrf2/TNF-α pathway.

The potential protective effect of modafinil in intestinal ischemic reperfusion-induced in rats.

OBJECTIVE: Intestinal ischemia reperfusion (IR) is a pathophysiologic process that leads to oxidative stress and acute inflammatory responses. Understanding the mechanisms explaining this inflammation is essential to developing therapeutic strategies. Therefore, the purpose of this study was to evaluate the protective outcome of modafinil (Mod) against intestinal damages caused by intestinal IR injury. METHODS/MATERIALS: Fourty adult Male Wistar rats were randomly divided into four groups: sham control group; intestinal IR group; Mod pre-treated IR group and Mod post-treated IR group. Mod in a dose of 10 mg/kg was injected intraperitoneally once daily for 7 days pre or post IR treatment. RESULTS: Mod significantly attenuated the IR induced elevations in intestinal malondialdehyde (MDA), nitric oxide (NO), tumor necrosis factor alpha (TNF-α), interleukin 1-ß (IL-1ß) and P-glycoprotein (P-gp) levels, caspase-3 activity. However, a significant increase in TAC was reported as compared with the IR group but its post-treated IR group was highly protective. Mod post-treatment down-regulated the IR induced cyclo-oxygenase-2 (COX-2) over-expression. Distorted mucosa with loss of surface epithelial cells, epithelial separation oedematous lamina propria and inflammatory cellular infiltration detected by histopathological examination of intestinal tissue, were markedly ameliorated by Mod post-treatment. On the other hand, Mod pre-treatment showed less protection against intestinal IR in rats. CONCLUSION: Current study suggests that Mod post-treatment ameliorated intestinal damages, so it can be considered a potential therapeutic agent to protect against the major clinical challenge of intestinal injury resulting from IR.

Hydrogen sulfide renal protective effects: possible link between hydrogen sulfide and endogenous carbon monoxide in a rat model of renal injury.

Hydrogen sulfide (H2S), along with nitric oxide (NO) and carbon monoxide (CO), proved to have renoprotective effects in various renal diseases. Therefore, this study investigated the renoprotective effect of H2S, in a renal injury model, and its crosstalk with other gasotransmitters such as CO. Thirty-two adult rats were divided into four groups: control, gentamicin (GEN)-treated, GEN + sodium hydrosulfide (NaHS), and GEN + NaHS + zinc protoporphyrin (ZnPP) groups. GEN was used to induce renal injury, NaHS is a water-soluble H2S, and ZnPP is a selective heme oxygenase-1 (HO-1) inhibitor used to inhibit CO synthesis in vivo. NaHS improved kidney functions in the GEN group as evidenced by significantly lower levels of renal injury markers: serum urea, creatinine, uric acid, urinary albumin excretion, and urinary albumin/creatinine. Moreover, NaHS administration to the GEN-treated group significantly lowered renal levels of NO and tumor necrosis factor-α with an increase in total antioxidant, HO-1, and interleukin-10 levels. Furthermore, NaHS administration downregulated the GEN-induced overexpression of the renal inducible nitric oxide synthase (iNOS) and upregulated the suppression of endothelial nitric oxide synthase (eNOS) with improvement in the histological examination and periodic acid Schiff (PAS) staining. However, this improvement in kidney function produced by NaHS was reduced by combination with ZnPP but still improved as compared with the GEN-treated group. The renoprotective effects of H2S can be through its effects on renal tissue antioxidants, pro-inflammatory and anti-inflammatory cytokines, and expression of eNOS and iNOS which can be partially dependent on CO pathway via induction of HO-1 enzyme.

Possible protective effect of platelet-rich plasma on a model of cisplatin-induced nephrotoxicity in rats: A light and transmission electron microscopic study.

BACKGROUND: Cisplatin (Cis), is a potent chemotherapeutic drug. However, Cis nephrotoxicity is high, thus limiting its use. Platelet-rich plasma (PRP) is an autologous product, easy to get from blood centrifugation. The aim of this study is to investigate the effects of PRP in reversing Cis-induced nephrotoxicity. MATERIALS AND METHODS: Thirty-two adult albino rats were distributed into Group I, the control group; Group II, in which the rats received Cis (5 mg·kg-1 ·day -1 , intraperitoneal); Group III and Group IV, in which the rats received Cis, followed by normal saline and PRP distribution, respectively (1 ml) over the renal surface 24 hr later. All rats were killed on the eighth day of the experiment. Histopathological changes were examined. RESULTS: Glomerular atrophy, tubular degeneration, interrupted PAS reaction, highly expressed caspase-3, and ultra-structural changes were observed after Cis injection, which improved with PRP administration. CONCLUSION: PRP reduced acute kidney injury through the epithelial GFs.

Protective effects of either C-peptide or l-arginine on pancreatic ß-cell function, proliferation, and oxidative stress in streptozotocin-induced diabetic rats.

Diabetes and cardiometabolic risk factors including hypertension and dyslipidemia are the major threats to human health in the 21st century. Apoptosis in pancreatic tissue is one of the major causes of diabetes type 1 progression. The aim of this study was to investigate the effects of C-peptide or l-arginine on some cardiometabolic risk factors, pancreatic morphology, function and apoptosis, and the mechanisms of their actions. Forty adult male albino rats were divided into four equal groups: 1-control nondiabetic, 2-diabetic (no treatment), 3-diabetic + C-peptide, and 4-diabetic + l-arginine. Diabetes was induced by a single intraperitoneal injection of high dose streptozotocin. At the end of the experiment, sera glucose, insulin levels, total antioxidant capacity (TAC), malondialdehyde (MDA), nitric oxide (NO), and pancreatic MDA, TAC, and B-cell lymphoma 2 were measured. The morphology and proliferating activity of the pancreas were examined by hematoxylin and eosin histological stain, proliferative cell nuclear antigen (PCNA), and insulin antibodies. Our results showed that induction of diabetes caused hyperglycemia, dyslipidemia, and oxidative stress. However, administration of C-peptide or l-arginine significantly improved the pancreatic histopathology with a significant increase in the area % of insulin immunoreactivity, the number of PCNA immunopositive cells, the number of islets, and the diameter of islets compared with the diabetic group. C-peptide treatment of the diabetic rats completely corrected these errors, while l-arginine partially antagonized the above diabetic complications. So the administration of C-peptide as an adjuvant therapy in type 1 diabetes can significantly decrease apoptosis of pancreas and subsequent progression of diabetes complication.

Morphometry of suprascapular notch in Egyptian dry scapulae and its correlation with measurements of suprascapular nerve safe zone for clinical consideration

The suprascapular notch is bridged by a superior transverse scapular ligament (STSL) and serves as a passage for the suprascapular nerve. The purpose of this study was to group suprascapular notches (SSN) and provide data on the association of the safe zone distances of the suprascapular nerve. Sixty-five Egyptian dried scapulae were classified into five groups; measurement of dimensions of SSN and measurement of safe zone for the suprascapular nerve were taken. The collected data were analyzed and the correlated parameters in the prevalent types of notches were done.Scapulae were classified into five groups of which the most prevalent groups were Type III (47.63%) followed by Type I (40%). The mean measurements of 'safe zone' distances vary according to the type of notch and correlate with notch dimensions. The present work displayed the anatomical variants of SSN and analyzed the measurement of safe zone distances to help the clinicians to manage different pathological conditions of the shoulder, in order to avoid iatrogenic injury

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Evidence of the protective effect of l-arginine and vitamin D against monosodium glutamate-induced liver and kidney dysfunction in rats.

Monosodium glutamate (MSG) is frequently consumed as a flavor enhancer or food additive. Possible MSG-induced injurious effects on some organs have been stated in experimental animal models. Thus, in this study we tried to clarify effect and possible mechanism of action of MSG on liver and kidney, and if this results affected by the addition of l-Arginine or vitamin D to it. Animals divided into; Control, MSG treated, MSG + vitamin D treated, MSG + L-arginine treated group. Serum separated to determine liver and kidney function parameters. Kidneys and livers dissected out for histological examination and for assay of oxidative stress markers. RESULTS: MSG increased body weight and produced liver and kidney dysfunctions. The MSG-induced oxidative liver and kidney damage was proved. Vitamin D and l- Arginine have been shown to protect and restore the liver and the kidney capabilities in MSG models injury via inhibiting oxidative damage, vitamin D or l- Arginine suppresses the increased food intake and body weight gain induced by MSG. CONCLUSIONS: due to injurious effect of MSG, it should be avoided especially in liver or kidney disorders, foods containing excess MSG can be fortified with vitamin D or l- Arginine to overcome its adverse effects.