Ameliorating effect of troxerutin in unilateral ureteral obstruction induced renal oxidative stress, inflammation, and apoptosis in male rats

Unilateral ureteral obstruction (UUO) induces renal injury and troxerutin attenuates the inflammatory parameters and decreases oxidative stress. Accordingly, this study explored the renoprotective effect of troxerutin in UUO-induced renal oxidative stress, inflammation, and apoptosis in male Wistar rats. Animals were randomly separated into five groups (n = 8): control, UUO, and three UUO groups treated with troxerutin (1, 10, and 100 mg/kg). UUO-induced and vehicle/troxerutin administration was continued for 3 days. Then serum creatinine, mean arterial pressure (MAP), renal perfusion pressure (RPP), renal vascular resistance (RVR), and renal blood flow (RBF) were measured. Superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase activities, total antioxidant capacity (TAC), and malondialdehyde (MDA) levels as some oxidative stress parameters were measured in the left kidney. The immunoblotting method was applied to evaluate the cleaved caspase-3 Bax, Bcl-2, and TNF-α proteins level. The hematoxylin and eosin method was used to assess the kidney tissue damage score (KTDS). In 3 days, UUO significantly increased serum creatinine level, KTDS, RVR, MDA, Bax, cleaved caspase-3, and TNF-α protein levels (p < 0.05); and decreased RBF, TAC, SOD, catalase, GPx activity levels and Bcl-2 protein expression level in the left kidney (p < 0.05). Troxerutin (100 mg/kg) significantly attenuates the indicators alteration induced by UUO. Our findings represented that the renoprotective effect of troxerutin may be related to its anti-oxidative stress, anti-inflammation, anti-apoptosis, and RBF improver properties. © 2020, Springer-Verlag GmbH Germany, part of Springer Nature

The therapeutic approaches of renal recovery after relief of the unilateral ureteral obstruction: A comprehensive review

Unilateral ureteral obstruction (UUO) as a clinical disorder can cause renal damage. The permanent injury occurs if the obstruction is not relieved. Renal injury can be reversed with UUO removal (RUUO). RUUO attenuates the renal hemodynamic and functional impairment and decreases the renal fibrosis and apoptosis. Nevertheless, kidney injury may continue after RUUO, and synchronous medication therapy seems necessary. However, UUO and post-RUUO periods are also important in final renal recovery. To date, various therapeutic strategies have been applied to develop renal recoverability after RUUO. In animal studies, the effect of some pharmacological agents such as mesenchymal stem cells, anti-inflammation drugs, L-arginine, bone morphogenetic protein-7, epidermal growth factor, allopurinol, renin-angiotensin system antagonists, and endothelin A/B receptor blocker were surveyed in RUUO model. Also, post-RUUO renal recoverability has been studied in human researches. In these studies, the effective strategies have focused on surgery for RUUO creation via urethrotomy, urethroplasty, stent balloon dilatation, and stenting. Accordingly, in this review, we focused on the therapeutic procedure of renal recovery after the RUUO situation in human and animal studies. © 2020 University of Baghdad-College of Science. All rights reserved

The effect of hydroalcoholic extract of Pistacia vera on pentylenetetrazole-induced kindling in rat

Background and objectives: Most antiepileptic drugs that are commonly being used in the clinic have a wide range of unwanted side effects; while some species of pistachioshave been used in the traditional medicine to treat epilepsy. The aim of the present study was to investigate the anticonvulsant effects of the hydroalcoholic extract of Pistacia vera L. in pentylenetetrazole (PTZ)-induced chemical kindling. Methods: this study was carried out on 40 male Wistar rats. Chemical kindling was induced by intraperitoneal administration of PTZ (40 mg/kg) on every alternate day (30 days). The hydroalcoholic extract of P. vera (50 and 100 mg/kg) were administered orally every day (30 days). In days which animals received both PTZ and extract, PTZ was injected 30 min after extract administration. Convulsive behavior was observed for 30 min after PTZ injection and scored according to racine scale. Diazepam was used as the reference anticonvulsant drug. Results: Pretreatment with 50 and 100 mg/kg of P. vera extract decreased seizure scores, stage 4 latency and stage 5 duration compared to the control group. The anti-epileptic effects of P. vera extract were comparable to diazepam. Conclusion: The present findings demonstrated that the hydroalcoholic extract of P. vera may inhibit the development of seizure behavior following chronic PTZ-induced model of epilepsy in rats

The effect of hydroalcoholic extract of Pistacia vera on pentylenetetrazole- induced kindling in rat

Abstract Background and objectives: Most antiepileptic drugs that are commonly being used in the clinic have a wide range of unwanted side effects; while some species of pistachios have been used in the traditional medicine to treat epilepsy. The aim of the present study was to investigate the anticonvulsant effects of the hydroalcoholic extract of Pistacia vera L. in pentylenetetrazole (PTZ)-induced chemical kindling. Methods: this study was carried out on 40 male Wistar rats. Chemical kindling was induced by intraperitoneal administration of PTZ (40 mg/kg) on every alternate day (30 days). The hydroalcoholic extract of P. vera (50 and 100 mg/kg) were administered orally every day (30 days). In days which animals received both PTZ and extract, PTZ was injected 30 min after extract administration. Convulsive behavior was observed for 30 min after PTZ injection and scored according to racine scale. Diazepam was used as the reference anticonvulsant drug. Results: Pretreatment with 50 and 100 mg/kg of P. vera extract decreased seizure scores, stage 4 latency and stage 5 duration compared to the control group. The anti-epileptic effects of P. vera extract were comparable to diazepam. Conclusion: The present findings demonstrated that the hydroalcoholic extract of P. vera may inhibit the development of seizure behavior following chronic PTZ-induced model of epilepsy in rats

Ceftriaxone improves hepatorenal damages in mice subjected to D-galactose-induced aging

Ceftriaxone (CTX) is a third-generation cephalosporin antibiotic that has broad-spectrum antimicrobial activity. This agent also has anti-inflammatory and antioxidant characteristics. In the current study, the effects of CTX against hepatorenal damages in a D-galactose (DGL) induced aging model were investigated. We used twenty-eight male mice which equally and randomly were separated into four groups as follows: Control, DGL group (treated with 500 mg/kg/day DGL orally for six weeks), DGL + CTX group (treated with 500 mg/kg/day DGL orally plus 200 mg/kg/day CTX intraperitoneally for six weeks), and CTX group (treated with 200 mg/kg/day CTX intraperitoneally for six weeks). The liver and kidney function indices such as serum creatinine, blood urine nitrogen, alanine aminotransferase, and aspartate aminotransferase were measured. Also, levels of malondialdehyde, catalase, and glutathione peroxidase in hepatic and renal tissues were evaluated. Moreover, the expression profiles of interleukin 1 beta and tumor necrosis factor alpha were assessed. The liver and kidney tissues were assessed for histopathological lesions. The results showed that aging induced by DGL leads to abnormalities in functional indices of the liver and kidneys. DGL also induced significant oxidative stress and inflammation, as well as histopathological lesions, in these organs. CTX improved functional indices, as well as the parameters of oxidative stress and inflammation, compared with the DGL-treated animals. These results were also confirmed by histological evaluations of the liver and kidneys. These data provide evidence for the therapeutic value of CTX in clinical practice for mitigating the hepatorenal damages of aging. © 2020 Elsevier Inc

Long-term metformin therapy improves neurobehavioral functions and antioxidative activity after cerebral ischemia/reperfusion injury in rats

Metformin (MET),an antidiabetic drug, has shown antioxidative and neuroprotective effects. In the present investigation, we aimed to study the probable effects of MET on cerebral ischemia/reperfusion in rats. Rats underwent cerebral ischemia/reperfusion and MET was administered orally at doses of 100 and 200 mg/kg for 56 days. Anxiety- and depressive-like behaviors were evaluated by elevated plus-maze or forced swimming tests, respectively. was assessed by. Cognitive functions were assessed by Y-maze continuous alternation task and morris water maze. The activity of SOD and the level of BDNF were measured in brains samples. Our results showed that administration of 200 mg/kg MET reduced the percent of brain edema (84.00 ± 2.13) in comparison with the ischemic animals (91.25 ± 2.25) (p < 0.05). Administration of 200 mg/kg MET in ischemic animals improved anxiety-like behavior by increasing the percentage of the open arms entries (46.51 ± 3.13) and the percentage of the open arms time (32.70 ± 2.49) in comparison with the cerebral ischemia group (26.35 ± 7.02 and 15.32 ± 5.78, respectively) (all p < 0.001). MET treatment (200 mg/kg) increased the cognition index of correct alternations (90.20 ± 4.95) in comparison with the cerebral ischemia group (59.50 ± 8.01) (p < 0.05). MET at the both doses reduced escape latency compared to the cerebral ischemia animals (all p < 0.05). In addition, 200 mg/kg MET increased the time spent in the target quadrant (16.06 ± 0.58) in comparison with the ischemic animals (9.84 ± 0.92) (p < 0.001) and the both doses of the drug increased the number of crossing (5.42 ± 0.36 and 6.5 ± 0.42, respectively) compared to the cerebral ischemia group (3.75 ± 0.31) (p < 0.05 and p < 0.001, respectively). Moreover, 200 mg/kg MET reduced the immobility time (47.50 ± 9.00) in comparison with the cerebral ischemia group (93.43 ± 8.28) (p < 0.001). Furthermore, the both doses of MET increased the BDNF levels (4590 ± 197.6 and 4767 ± 44.10, respectively) in comparison with the ischemic animals (3807 ± 42.56) (p < 0.01 and p < 0.001, respectively). Also, the both doses of the drug increased the SOD activity of brain (52.67 ± 0.33 and 55.00 ± 0.57, respectively) compared to the ischemic animals (49.33 ± 0.33) (p < 0.01 and p < 0.001, respectively). Based on our data, long-term MET therapy may improve behavioral disorders following cerebral ischemia/reperfusion and can be considered as a novel therapeutic approach for the treatment of brain ischemic conditions. © 2020 Elsevier Inc