Minia University

About: Minia University is a education organization based out in Minya, Egypt. It is known for research contribution in the topics: Population & Medicine. The organization has 4967 authors who have published 8986 publications receiving 108384 citations.

Protective effect of peroxisome proliferator activator receptor (PPAR)-α and -γ ligands against methotrexate-induced nephrotoxicity.

Abstract: Context: The anticancer drug methotrexate (MTX) may cause multi-organ toxicities, including nephrotoxicity.Objective: To investigate effects of peroxisome proliferator activator receptor (PPAR)-α and -γ agonists; fenofibrate (FEN) and pioglitazone (PIO), in MTX-induced nephrotoxicity in rats.Methods: Rats were given FEN or PIO (150 or 5 mg/kg/day, respectively) orally for 15 days. MTX was injected as a single dose of 20 mg/kg, i.p. at day 11 of experiment, with or without either PPAR agonists.Results: MTX induced renal toxicity, assessed by increase in serum urea and creatinine as well as histopathological alterations. MTX caused renal oxidative/nitrosative stress, indicated by decrease in GSH and catalase with increase in malondialdehyde and nitric oxide (NOx) levels. In addition, MTX increased renal level of the pro-inflammatory cytokine; tumor necrosis factor (TNF)-α and up-regulated the expression of both the inflammatory and apoptotic markers; NF-κB and caspase 3. Pre-administration of FEN or...

Surveillance of acute hepatitis C in Cairo, Egypt.

Abstract: Surveillance of acute hepatitis has been set up in two fever hospitals in Cairo to diagnose acute hepatitis C. Patients were categorized as definite acute hepatitis C with positive hepatitis C virus (HCV) RNA and without anti-HCV antibody, or probable acute hepatitis C with positive HCV RNA, positive anti-HCV antibody, alanine aminotransferase >/=4 times the upper limit of normal (ULN), and high risk parenteral exposure in the 1--3 months prior to the beginning of symptoms. From May to November 2002, 315 patients were recruited in the study. Of these, 115 (36.5%) had acute hepatitis A, 89 (28.3%) had acute hepatitis B, and 111 (35.2%) had non-A non-B acute hepatitis. Of the total with complete data (n=309), 12 (3.9%, 95% CI=2.0%-6.7%) had definite acute hepatitis C, and 11 (3.6%, 95% CI=1.8%-6.3%) had probable acute hepatitis C. In patients with definite acute hepatitis C, dental exposure (n=5) and intravenous drug use (n=2), were the only high risk procedures found in the 6 months prior to diagnosis. Five patients had no identifiable parenteral exposure. In conclusion, results from this study suggest that acute hepatitis C can be diagnosed by surveillance of acute hepatitis in hospital settings in Cairo and that minor community exposures contribute substantially to local HCV transmission.

In-silico drug repurposing and molecular dynamics puzzled out potential SARS-CoV-2 main protease inhibitors.

Abstract: Herein, the DrugBank database which contains 10,036 approved and investigational drugs was explored deeply for potential drugs that target SARS-CoV-2 main protease (Mpro). Filtration process of the database was conducted using three levels of accuracy for molecular docking calculations. The top 35 drugs with docking scores > -11.0 kcal/mol were then subjected to 10 ns molecular dynamics (MD) simulations followed by molecular mechanics-generalized Born surface area (MM-GBSA) binding energy calculations. The results showed that DB02388 and Cobicistat (DB09065) exhibited potential binding affinities towards Mpro over 100 ns MD simulations, with binding energy values of -49.67 and -46.60 kcal/mol, respectively. Binding energy and structural analyses demonstrated the higher stability of DB02388 over Cobicistat. The potency of DB02388 and Cobicistat is attributed to their abilities to form several hydrogen bonds with the essential amino acids inside the active site of Mpro. Compared to DB02388 and Cobicistat, Darunavir showed a much lower binding affinity of -34.83 kcal/mol. The present study highlights the potentiality of DB02388 and Cobicistat as anti-COVID-19 drugs for clinical trials. Communicated by Ramaswamy H. Sarma.

Empagliflozin attenuates transient cerebral ischemia/reperfusion injury in hyperglycemic rats via repressing oxidative–inflammatory–apoptotic pathway

Abstract: Hyperglycemia is one of the ischemic neuronal damage triggers that exacerbate the response to oxidative stress, inflammation, and apoptosis induced by cerebral ischemia/reperfusion (I/R) injury. Empagliflozin, a sodium-glucose cotransporter 2 (SGLT 2) inhibitor, was shown to effectively reduce hyperglycemia and glucotoxicity besides improving glycemic control in diabetics. Therefore, the present study was conducted to investigate the neuroprotective effect of empagliflozin against cerebral I/R injury in hyperglycemic rats. Hyperglycemia was induced by streptozotocin (55 mg/kg), and transient cerebral I/R was induced by bilateral common carotid occlusion for 30 min followed by 24-h reperfusion. Either empagliflozin (10 mg/kg; i.p.) or gliclazide (2 mg/kg, p.o.) was administered at 1 and 24 h after reperfusion. Treatment with empagliflozin showed a significant amelioration of behavioral/neurological functions and histopathological changes observed in brain tissues of hyperglycemic rats subjected to cerebral I/R injury. Comparable to gliclazide, empagliflozin decreased cerebral infarct volume along with suppression of cerebral oxidative stress, inflammatory, and apoptotic markers in brain tissues of hyperglycemic I/R-injured rats. These findings suggested that empagliflozin can significantly alleviate neuronal damage resulting from global I/R injury induced in hyperglycemic rats. The proposed neuroprotective effect of empagliflozin may be attributed to its glycemic control effect and related antioxidant, anti-inflammatory, and antiapoptotic effects.