Abstract:Objective To assess the influence of oxidative stress on the gene expression of nitric oxide synthases (NOS 3 and NOS 2) and, hence, the cardiovascular responses in preeclampsia.
Methods This was a case control study in which patients with preeclampsia (PE group) and normal pregnancy controls (NP group) were included according to the guidelines of the American College of Obstetricians and Gynecologists (ACOG). The serum levels of malondialdehyde (MDA), total antioxidant capacity, and nitric oxide (NO… Show more
“…cDNA was amplified with quantitative reverse transcription-PCR ( Kong et al, 2021 ). The gene expression of NMDAR and Tau protein are presented as fold change calculated by using the formula 2^-ΔΔCq ( Herur et al, 2022 ). PCR primers specific to each gene are as depicted in Table 1 .…”
Present study aimed to assess effect of pre-treatment with Mucuna pruriens seed extract and its bioactive molecule(s) on NMDAR and Tau protein gene expression in cerebral ischemic rodent model. Methanol extract of M. pruriens seeds was characterized by HPLC, and β-sitosterol was isolated by flash chromatography. In vivo studies to observe the effect of pre-treatment (28 days) with methanol extract of M. pruriens seed and β-sitosterol on the unilateral cerebral ischemic rat model. Cerebral ischemia induced by left common carotid artery occlusion (LCCAO) for 75 min (on day 29) followed by reperfusion for 12 h. Rats (n = 48) divided into four groups. GroupI (control,Untreated + LCCAO)-No pre-treatment + cerebral ischemia; GroupII(β-sitosterol + Sham)-pre-treatment with β-sitosterol, 10 mg/kg/day + sham-operated; GroupIII(β-sitosterol + LCCAO)-pre-treatment with β-sitosterol, 10 mg/kg/day + cerebral ischemia; GroupIV(methanol extract + LCCAO)-pre-treatment with methanol extract of M. pruriens seeds, 50 mg/kg/day + cerebral ischemia. Neurological deficit score was assessed just before sacrifice. Experimental animals were sacrificed after 12 h reperfusion. Brain histopathology was performed. Gene expression of NMDAR and Tau protein of left cerebral hemisphere (occluded side) was performed by RT-PCR. Results revealed that the neurological deficit score was lower in groups III and IV compared to group I. NMDAR and tau protein mRNA expression in left cerebral hemisphere were upregulated in Group I, downregulated in groups III and IV. Histopathology of left cerebral hemisphere (occluded side) in Group I showed features of ischemic brain damage. Groups III and IV, left cerebral hemisphere showed less ischemic damage compared GroupI. Right cerebral hemisphere showed no areas of ischemia-induced brain changes. Pre-treatment with β-sitosterol and methanol extract of M. pruriens seeds may reduce ischemic brain injury following unilateral common carotid artery occlusion in rats.
“…cDNA was amplified with quantitative reverse transcription-PCR ( Kong et al, 2021 ). The gene expression of NMDAR and Tau protein are presented as fold change calculated by using the formula 2^-ΔΔCq ( Herur et al, 2022 ). PCR primers specific to each gene are as depicted in Table 1 .…”
Present study aimed to assess effect of pre-treatment with Mucuna pruriens seed extract and its bioactive molecule(s) on NMDAR and Tau protein gene expression in cerebral ischemic rodent model. Methanol extract of M. pruriens seeds was characterized by HPLC, and β-sitosterol was isolated by flash chromatography. In vivo studies to observe the effect of pre-treatment (28 days) with methanol extract of M. pruriens seed and β-sitosterol on the unilateral cerebral ischemic rat model. Cerebral ischemia induced by left common carotid artery occlusion (LCCAO) for 75 min (on day 29) followed by reperfusion for 12 h. Rats (n = 48) divided into four groups. GroupI (control,Untreated + LCCAO)-No pre-treatment + cerebral ischemia; GroupII(β-sitosterol + Sham)-pre-treatment with β-sitosterol, 10 mg/kg/day + sham-operated; GroupIII(β-sitosterol + LCCAO)-pre-treatment with β-sitosterol, 10 mg/kg/day + cerebral ischemia; GroupIV(methanol extract + LCCAO)-pre-treatment with methanol extract of M. pruriens seeds, 50 mg/kg/day + cerebral ischemia. Neurological deficit score was assessed just before sacrifice. Experimental animals were sacrificed after 12 h reperfusion. Brain histopathology was performed. Gene expression of NMDAR and Tau protein of left cerebral hemisphere (occluded side) was performed by RT-PCR. Results revealed that the neurological deficit score was lower in groups III and IV compared to group I. NMDAR and tau protein mRNA expression in left cerebral hemisphere were upregulated in Group I, downregulated in groups III and IV. Histopathology of left cerebral hemisphere (occluded side) in Group I showed features of ischemic brain damage. Groups III and IV, left cerebral hemisphere showed less ischemic damage compared GroupI. Right cerebral hemisphere showed no areas of ischemia-induced brain changes. Pre-treatment with β-sitosterol and methanol extract of M. pruriens seeds may reduce ischemic brain injury following unilateral common carotid artery occlusion in rats.
“…Восстановление обмена ХС и противодействие окислительным процессам приводит к возрастанию уровня и доступности L-аргинина для еNOS и, соответственно, повышению содержания NOх. Такого плана исследования представлены в литературе; в них установлено, что экспрессия NOS-3 снижается при повышении содержания МДА [17]. Полученные данные показали снижение концентрации МДА в слоях интерстиция почек и печени под влиянием фабоматизола.…”
Section: сибирский журнал клинической и экспериментальной медициныunclassified
The conducted study indicates the priority use of the drug fabomatizole to protect living systems from the negative effects of lead acetate.Aim: To study the mechanisms of fabomatizole effect on the nature of changes in redox reactions, NO-forming function of the endothelium, cholesterol metabolism and functional parameters in rats with lead intoxication.Material and Methods. The study was carried out on 60 Wistar rats. Lead intoxication was induced by intramuscular administration of lead acetate at a dose of 5 mg/kg of animal weight for a month. At the end of the intoxication period, Fabomatizol was administered at a dose of 10 mg/kg for a month. Next, blood and tissue samples were taken from rats to determine the activity of oxidative, antioxidant, enzymatic systems, nitric oxide metabolism, and blood lipid spectrum.Results. The data obtained showed that intramuscular administration of fabomatisol in case of lead intoxication has an antioxidant effect and inhibits lipid peroxidation (LPO) activity. Under the influence of fabomatizol, nitric oxide metabolism andtotal nitric oxide metabolites (NOx) content significantly increased, and a negative correlation was found between the malondialdehyde level, superoxide dismutase activity and NOx. At the same time, the study found a decrease in the expression level of eNOS as the cause of a reduced concentration of NOx in the blood. L-arginine availability for eNOS was disturbed by atherogenic low density lipoprotein (LDL). Treatment with fabomatizol against the background of lead intoxication caused a decrease in total cholesterol, LDL cholesterol and an increase inhigh density lipoprotein cholesterol. By inhibiting lipid peroxidation in the cells of the renal and hepatic tissues, fabomatizol contributed to the restoration of lipid-protein interactions and the functional activity of Na and K-activated ATPase in the renal interstitium. Simultaneously, there is an activation of Na,K-ATP-ase in the hepatocyte and a decrease in the level of organ-specific enzymes in the blood plasma.Conclusion. The results obtained are evidence of the antioxidant properties of fabomatisol in lead intoxication, its ability to induce the activity of antioxidant system (AOS enzymes, stimulate the NO-forming function of the endothelium, NOx production and the activity of the membrane enzyme – Na,K-ATP-ase in the renal and hepatic tissues and reduce the level of organ-specific enzymes in blood plasma.
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