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Background: Organ ischemia-reperfusion (IR) is a common clinical condition associated with various situations such as trauma surgery, organ transplantation, and myocardial ischemia. Current therapeutic methods for IR injury have limitations, and nanotechnology, particularly zinc oxide nanoparticles (ZnO NPs), offers new approaches for disease diagnosis and treatment. In this study, we investigated the protective and anti-apoptotic effects of ZnO NPs in liver ischemia-reperfusion (IR) injury in rats. Methods: Forty-eight male rats were divided into six groups: sham, ZnO5, ZnO10, ischemiareperfusion (IR), IR+ZnO5, and IR+ZnO10. The protective effect of ZnO NPs was evaluated by liver enzymes (AST, ALT, Bilirubin, ALP), biochemical (TAC, TNF-a, and MDA), molecular examinations (Bcl2, BAX), and histopathological evaluations (H&E, TUNEL). Results: Pre-treatment with ZnO5 and ZnO10 improved hepatic function in IR liver injury, attenuated the levels of oxidants (P = 0.03) and inflammatory mediators, and reduced apoptosis (P = 0). ZnO10 was found to have a greater effect on ischemic reperfusion injury than ZnO5 did. Histopathological examination also showed a dose-dependent decrease in alterations in the IR+ZnO5 and IR+ZnO10 groups. Conclusion: Administration of ZnO5 and ZnO10 improved liver function after IR. The findings of this study suggest that ZnO NPs have a protective effect against oxidative stress and apoptosis in liver ischemia-reperfusion injury in rats. These results may have important implications for developing advanced methods in ischemia-reperfusion treatment. [ABSTRACT FROM AUTHOR]

Background: COVID-19 has become a serious health problem worldwide. Objectives: The current study investigated the prognostic factors associated with demographical parameters, clinical and vital signs, and laboratory results for predicting severity and mortality in patients infected with COVID-19. Methods: This retrospective analysis was conducted on the medical records of 372 COVID-19-positive patients hospitalized at the Khatam al-Anbiya Hospital, Shoushtar, Iran, from Sep 2020 to Sep 2021. The association of demographic parameters, clinical and vital signs, and laboratory results with severity and patients' outcomes (survival/mortality) was studied. The patients were divided into the non-severe group (n = 275) and the severe group (n = 97). COVID-19 disease severity was determined based on the severity of pulmonary involvement using CT chest images. The collected data were analyzed using IBM SPSS software for Windows (version 18). Logistic regression analysis was employed using the Forward LR method to predict COVID-19 severity and mortality. Results: The rates of mortality and the severe form of the disease were 87.1% (n = 324) and 12.9% (n = 48), respectively. A prognostic value was observed in predicting COVID-19 severity and mortality for some clinical and vital signs (diabetes (P < 0.001, P = 0.019), hypertension (P = 0.024, P= 0.012), pulmonary diseases (P= 0.038, P< 0.001), and anosmia (P = 0.043, P = 0.044) and paraclinical parameters (FBS(P = 0.014, P = 0.045), BUN (P= 0.045,0.001), Cr (P = 0.027, P = 0.047), Neut(P = 0.002, P = 0.005), and SpO2 (P= 0.014, P = 0.001)). Cardiovascular disorders (P = 0.037), fever (P = 0.008), and dyspnea (P= 0.020) were also effective at predicting disease- related mortality. Multiple logistic regression analyses showed that diabetes disease, the place of residence, PCO2, and BUN with R2 = 0.18, and age, pulmonary diseases, and BUN with R2 = 0.21 were involved in predicting the severity and mortality, respectively. Conclusions: It seems that in addition to the BUN, diabetes and pulmonary diseases play a more significant role in predicting the severity and mortality due to COVID-19, respectively. [ABSTRACT FROM AUTHOR]

Introduction: Acrylamide (ACR) is a toxic substance that has renal toxicity. We aim to investigate the therapeutic activity of ellagic acid (EA) on renal injury induced by ACR in Wistar rats. Methods: Thirty-five male Wistar rats were assigned into 5 groups: the control group (5ml/ kg normal saline), the ACR group (20mg/kg ACR), the ACR+EA10 group (ACR and 10mg/ kg EA), the ACR+EA30 group (ACR and 30mg/kg EA) and the EA30 group (30mg/kg EA). ACR and EA were daily administered by gavage for 30 days. Renal function was assessed by measuring the sera levels of creatinine (Cr) and blood urea nitrogen (BUN). Renal oxidative and inflammatory markers including malondialdehyde (MDA), nitric oxide (NO), protein carbonyl (PC), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). hematoxylin and eosin staining was employed to assess pathological alternations of the kidney. Results: EA (more potentially 30mg/kg) administration alleviated the ACR-induced alterations in Cr and BUN levels. Moreover, EA treatment reduced the elevated levels of MDA, NO and PC as well as TNF-α and IL-1β content in renal tissue. Furthermore, reduced activity of SOD and CAT as well as GSH content in the kidney was increased by EA treatment. EA attenuated the ACR-induced pathological alterations in kidney. Conclusion: These findings suggested that EA could mitigate ACR-induced kidney injury due to its potent antioxidant and anti-inflammatory effects. [ABSTRACT FROM AUTHOR]

Chronic exposure to toxic inorganic arsenic results in the adverse health effects including skin lesions, cardiovascular diseases, diabetes, neurological disorders, and liver and kidney diseases. Gallic acid (GA) is an important phenolic compound, which could protect different tissues from oxidative stress induced damage. The present study investigated effects of GA against sodium arsenite (SA)-induced renal and hepatic toxicity. Thirty-five rats were randomly divided in to five groups; group 1 was treated with normal saline (2 ml/kg/day, p.o.; for 21 days); group 2 was exposed to SA (10 mg/kg/day, p.o.; for 14 days); groups 3 and 4 were treated with GA (10 and 30 mg/kg/day, respectively; for 7 days) prior to exposure to SA, and treatment was continued up to 21 days in parallel with SA administration; group 5 was treated with GA (30 mg/kg/day, p.o.; for 21 days). The level of MDA, IL-1β, NO and glutathione (GSH) and the activity of glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) were evaluated in kidney and liver tissues. Histopathological parameters and serum levels of ALT, AST, ALP, Cr and BUN were also assessed. Treatment with GA remarkably improved SA-induced alteration of hematological and histopathological parameters; these protective effects were associated with the reduction of SA-induced elevation of MDA, IL-1β and NO levels as well as reduction of GSH level and GPx, SOD and CAT activity. Our results suggest that GA may inhibit SA-induced kidney and liver toxicity through scavenging reactive free radicals and increasing intracellular antioxidant capacity. [ABSTRACT FROM AUTHOR]