Background
Epilepsy is a common disorder affecting approximately 50 million people worldwide. Oxidative stress is known to play an important role in the pathophysiology of diseases, including ...epilepsy. In this study, we investigated the effects of sennoside B on PTZ-induced seizures in rats.
Method
The rats were grouped into Group Electroencephalography and Group Behavioral. Both Groups were divided into eight subgroups, and these subgroups were compared in terms of the time of first myoclonic jerk, Racine’s Convulsion Scale, malondialdehyde levels, and brain superoxide dismutase activity. The experimental seizure model was performed with pentylenetetrazol.
Results
The spike percentage was significantly lower in groups that received sennoside B, and this beneficial effect was shown to be associated with the dose of sennoside B received. The RCS score was lower and the FJM onset time was higher in the sennoside B-administered groups. Additionally, brain MDA and brain aquaporin-3 levels were lower and brain SOD activity was higher in the sennoside-administered groups.
Conclusions
The present study shows the beneficial effects of sennoside B on PTZ-induced convulsion in rats. It is considered that sennoside B which is a natural and safe product would be a good candidate for strengthening the management of epilepsy without serious side effects.
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•Oxytocin (i.p) ameliorates convulsions in a neonatal hypoxia/PTZ seizure model•Oxytocin (i.p) suppresses neuroinflammation and reduces hippocampal gliosis•Oxytocin (i.p) demonstrates ...anticonvulsant effect by increasing GABAergic activity
Previous studies have shown that, oxytocin has anticonvulsant and neuroprotective effects. One of the most important complications of Hypercapnic-hypoxia is drug resistance epilepsy. Effects of chronic intraperitoneal oxytocin treatment on gliosis, neuroinflammation and seizure activity was investigated in a model in which rats were exposed to hypoxia on postnatal day 1 and later challenged to the seizure-inducing pentylenetetrazol
Forty pups were included in the study on their first day of birth. 16 pups were exposed to 100% CO2 for 5 minutes and other 16 pups for 10 minutes. The remaining 8 pups comprised the control group. Groups were classified according to oxytocin administration within the first 4 weeks. Pentylenetetrazol was administered 6 months after the oxytocin treatment. The Racine’s Convulsion Scale and onset times of first myoclonic jerk (FMJ) were evaluated. To determine the mechanisms by which oxytocin exerted its effects on hypercapnic-anoxia exposed rats, we performed CA1 total neuron count & CA1 GFAP immunostaining, and measured brain levels of TNF-α and GAD-67.
The Racine scale and TNF-α values were significantly lower in both groups that received oxytocin, while time-to-FMJ and GAD-67 level were significantly higher. The histopathological evaluations showed that oxytocin had significant ameliorative effects (especially regarding gliosis) on the hippocampus of hypoxic rats.
Regarding the results of present study, it can be speculated that after acute hypercapnic-anoxia exposure, chronic Oxytocin treatment has long lasting therapeutic potential on rats, possibly by reducing the gliosis with its anti-inflammatory feature and by activating the GABA pathway.
Previous studies have established anti‐inflammatory, antioxidant, and neuroprotective effects of Exenatide in the central nervous system. Since these mechanisms are thought to have important roles in ...the pathophysiology of autism, we hypothesized that Exenatide may have healing effects in autism. We tested this hypothesis by examining the effects of Exenatide in an experimental autism model created by lipopolysaccharide (LPS) exposure in the womb, with behavioral tests, histopathological examinations, and biochemical measurements. The autism model was created by administration of LPS (i.p) to pregnant rats on the 10th day of their pregnancy at a dose of 100 µg/kg. On postnatal 21st day, a total of four groups were formed from offspring with regard to sex distribution and treatment. After a 45‐day treatment, behavioral analysis tests were performed on rats. Subsequently, the rats were sacrificed and biochemical analysis superoxide dismutase, tumor necrotizing factor alpha, nerve growth factor, 5‐hydroxyindoleacetic acid, and glutamic acid decarboxylase‐67 and histopathological analysis were performed. On the 10th day of the intrauterine period, LPS exposure was found to disrupt behavioral findings, increase inflammation and hippocampal gliosis, and decrease 5‐HIAA, GAD‐67, and NGF, especially in male rats. However, among the rats exposed to LPS in the intrauterine period, recipients of Exenatide demonstrated significant amelioration of findings. Exenatide therapy shows positive effects on behavioral disorders in an LPS‐induced autism model. This agent probably exerts its effects by suppressing inflammation and oxidative stress and reducing hippocampal gliosis. In addition, Exenatide has also been shown to positively affect cerebral serotonergic and GABAergic effects.
Exenatide has positive effects on behavioral disorders in LPS‐induced autism model. It reduced hippocampal gliosis. It exert its effects by suppressing inflammation and oxidative stress. It has positive effects on cerebral serotonergic and GABAergic activity.
Due to its rising global prevalence, liver failure treatments are urgently needed. Sinomenine (SIN), an alkaloid from sinomenium acutum, is being studied for its liver-repair properties due to ...Acetaminophen (APAP) overdose. SIN's effect on APAP-induced hepatotoxicity in rats was examined histologically and biochemically. Three groups of 30 adult male Wistar rats were created: control, APAP-only, and APAP + SIN. Histopathological and biochemical analyses were performed on liver samples after euthanasia. SIN is significantly protected against APAP damage. Compared to APAP-only, SIN reduced cellular injury and preserved hepatocellular architecture. The APAP + SIN Group had significantly lower ALT, MDA, and GSH levels, protecting against hepatocellular damage and oxidative stress. SIN also had dose-dependent antioxidant properties. When examining critical regulatory proteins, SIN partially restored Sirtuin 1 (SIRT1) levels. While BMP-7 levels were unaffected, histopathological evidence and hepatocyte damage percentages supported SIN's liver-restorative effect. SIN protected and repaired rats' livers from APAP-induced liver injury. This study suggests that SIN may treat acute liver damage, warranting further research into its long-term effects, optimal dosage, and clinical applications. These findings aid liver-related emergency department interventions and life-saving treatments.
Sepsis, a leading global cause of morbidity and mortality, involves multiple organ dysfunction syndromes driven by free radical-mediated processes. Uncontrolled inflammation in early sepsis stages ...can lead to acute lung injury (ALI). Activated leukocytes generate reactive oxygen species, contributing to sepsis development. Gallic acid, a phenolic compound, is known for its antimicrobial properties. This study aims to observe gallic acid's protective and restorative effect on the lungs in an experimental sepsis model. Male Wistar albino rats were subjected to a feces intraperitoneal injection procedure (FIP) to induce sepsis. Four groups were formed: normal control, FIP alone, FIP with saline, and FIP with gallic acid. Gallic acid was administered intraperitoneally at 20 mg/kg/day. Blood samples were collected for biochemical analysis, and computed tomography assessed lung tissue histopathologically and radiologically. Gallic acid significantly decreased malondialdehyde, IL-6, IL-1β, TNF-α, CRP levels, oxidative stress, and inflammation indicators. Lactic acid levels decreased, suggesting improved tissue oxygenation. Histopathological examinations revealed reduced lung damage in the gallic-acid-treated group. Computed tomography confirmed lower lung density, indicating less severe inflammation. Arterial blood gas analysis demonstrated improved oxygenation in gallic-acid-treated rats. Gallic acid exhibited anti-inflammatory and antioxidant effects, reducing markers of systemic inflammation and oxidative stress. The findings support its potential to protect against ALI during sepsis. Comparable studies underline gallic acid's anti-inflammatory properties in different tissues. Early administration of gallic acid in sepsis models demonstrated protective effects against ALI, emphasizing its potential as an adjunct therapy to mitigate adverse outcomes. The study proposes gallic acid to reduce mortality rates and decrease the need for mechanical ventilation during sepsis-induced ALI.
Peripheral nerve injuries inflict severe consequences, necessitating innovative therapeutic strategies. This study investigates the potential of liraglutide, a glucagon-like peptide-1 receptor ...agonist, in mitigating the consequences of peripheral nerve injury. The existing treatment methods for such injuries underscore the importance of ongoing translational research efforts. Thirty adult Wistar rats underwent sciatic nerve dissection and repair surgery. The nerves were surgically transected using micro scissors at a precise location located 1.5 cm proximal to the trifurcation site. The study included a control group and two experimental groups, one treated with saline (placebo group) and the other with liraglutide (experimental group) for 12 weeks. Motor function, electromyography (EMG), and biochemical and histopathological analyses were performed after 12 weeks of treatment. Electrophysiological assessments revealed that liraglutide improved the compound muscle action potential (CMAP) amplitude and motor function compared to the saline-treated group. Histological and immunohistochemical analyses demonstrated increased NGF expression, total axon number, and diameter and reduced fibrosis in the liraglutide group. Biochemical analyses illustrated liraglutide's antioxidative properties, evidenced by reduced malondialdehyde (MDA) levels. Galectin-3 levels were suppressed and GDF-11 levels were modulated by liraglutide, indicating anti-inflammatory and anti-apoptotic effects. Liraglutide is a promising therapeutic intervention for peripheral nerve injuries, promoting functional recovery and histopathological improvement. Its multifaceted positive impact, beyond glycemic control, suggests constructive effects on the acute and chronic inflammatory processes associated with peripheral neuropathy. These findings warrant further research to elucidate molecular mechanisms and facilitate clinical translation. The study contributes valuable insights to the growing understanding of GLP-1 receptor agonists' neuroprotective properties in the context of peripheral nerve injuries.
Alzheimer's disease (AD) is by far the most common cause of cognitive impairment in older adults. Current treatments are entirely focused on the symptoms of AD. A complex etiology for AD has been ...proposed recently, in which AD leads in elevated levels of inflammation. We previously studied digoxin's involvement in the sporadic-AD intracerebroventricular (ICV)-streptozotocin (STZ) animal model due to its anti-inflammatory and neuroprotective characteristics. 18 adult sprague–dawley rats were split into three groups: control (n = 6), STZ + Saline (n = 6), and STZ + Digoxin (n = 6). Twelve AD-induced rats were split into two groups using stereotaxy five days after STZ injection (3 mg/kg) into both lateral ventricles: one group got digoxin (0.1 mg/kg/day, i.p.) for three weeks, while the other group received saline. Following treatment, each subject was subjected to a passive avoidance learning (PAL) test, followed by brain tissue harvesting. The levels of tumor necrosis factor-alpha (TNF-α) and choline acetyl transferase (ChAT) were measured in the brain, and neurons were counted using Cresyl violet staining in cornu ammonis-1 (CA1) and cornu ammonis-3 (CA3) cornu ammonis (CA3). ICV-STZ significantly shortened PAL latency, increased brain TNF-α levels, decreased brain ChAT activity, and decreased hippocampus neuron number. On the other hand, digoxin significantly reduced all of these STZ-induced deleterious effects. Digoxin significantly rescued rats from memory loss caused by ICV-STZ by decreasing hippocampal cell death, neuroinflammation, and cholinergic deficiency. These findings suggest that digoxin may be beneficial in treating cognitive impairment and Alzheimer's disease.
This study aimed to evaluate the memory function in a rat model of fatty liver and to investigate the effects of statins on fatty liver, neuronal inflammation, oxidative stress and memory. In this ...study, 24 male rats were used and were divided into four groups consisting of 6 animals in each. Of them, 12 rats received liquid diet containing 35% fructose for 8 weeks in order to induce hepatosteatosis, while other animals had a normal nutrition. Group 1 served as controls and had a normal nutrition with no drug treatment. The animals in Group 2 had a normal nutrition and treated with atorvastatin. Group 3 received high-fructose diet with no drug treatment and Group 4 received high-fructose diet followed by atorvastatin treatment. After the two weeks of treatment period, passive avoidance tasks evaluating the memory were performed in both the study and control groups. The liver and brain were then removed for histologic, pathologic, and biochemical evaluation. In the non-treated rats with hepatosteatosis (Group 3), the lowest mean latency time and the highest mean histopathologic liver score, and brain TNF- α and MDA (Measurement of lipid peroxidation) were found (p < 0.00001). On the other hand, in the animals treated with atorvastatin, all these parameters were significantly higher than that of controls and significantly lower than that of Group 3 (p < 0.05). Fatty liver can increase inflammation and cause memory disorders, and atorvastatin may have a positive effect on cognitive disorders.
Recent studies suggest a possible link between type 2 diabetes and Alzheimer's disease (AD). Glucogan-like peptide 1 (GLP-1) facilitates insulin release from pancreas under hyperglycemic conditions. ...In addition to its metabolic effects, GLP-1 and its long-lasting analogs, including exenatide can stimulate neurogenesis and improve cognition in rodent AD model. The aim of the present study was to investigate the effects of exenatide on hippocampal cellularity, cognitive performance and inflammation response in a rat model of AD. Fourteen rats were used to create AD model using intracerebroventricular (ICV) streptozotocin (STZ) infusion while 7 rats were administered 0.9% NaCl only (sham-operated group). Following stereotaxic surgery, STZ received rats were randomly distributed into two groups, and treated with either saline or exenatide 20µgr/kg/day through intraperitoneally for two weeks. Then, cognitive performance (passive avoidance learning), brain tumor necrosis factor alpha (TNF-α) levels, choline acetyltransferase (ChAT) activity and hippocampal neuronal count were determined. While the brain TNF-α levels were significantly high in the saline-treated STZ group, exenatide treatment suppressed the increase in TNF-α levels. Saline-treated STZ group showed reduced ChAT activity compared to sham group. However, exenatide significantly preserved brain ChAT activity. The cognitive performance was also impaired in saline group while exenatide improved memory in rats. Moreover, exenatide treatment significantly prevented the decrease in hippocampal neurons. Overall, the results of the present study clearly indicated exenatide might have beneficial effects on impaired cognitive performance and hippocampal neuronal viability in AD by suppressing the inflammation response and increasing cholinergic activity.
