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Background Hyperlipidemia is a metabolic disorder that is caused by high levels of triglycerides and cholesterol in blood. Using of plants for the treatment of various ailments is a traditional practice in developing countries. The main objective of the study is to analyse the nutritional composition of Pistacia khinjuk and to assess its anti-hyperlipidemic activity. Materials and methods In the present study, the ethanolic extract of Pistacia khinjuk leaves was evaluated for antihyperlipidemic activity. 40 adult albino rats were divided into five groups. Hyperlipidemia was induced using high fat diet for 60 days. Pistacia khinjuk extract of 150 mg/kg body weight and 300 mg/kg of body weight was administered to the rats for 28 days. Proximate analysis of Pistacia khinjuk was also performed. Results Proximate analysis of Pistacia khinjuk leaves showed 6.8% ash content, 12.8% crude fiber and only 6.85% fat content. Findings of present study revealed that both doses of Pistacia khinjuk extract improved the serum lipid profile in albino rats by reducing total lipids, total cholesterol, triglycerides and low density lipoprotein, and increasing high density lipoprotein levels in Pistacia khinjuk treated groups. Body weight findings showed significant increase in body weight of all groups from zero day to 60th day. But before sacrifice, there was a decrease in hyperlipidemic and high dose Pistacia khinjuk while increase in control and low dose Pistacia khinjuk group respectively. Conclusion From the results of the present study, it is concluded that Pistacia khinjuk extract has curative effect against hyperlipidemia. [ABSTRACT FROM AUTHOR]

Epilepsy is an abiding condition associated with recurrent seizure attacks along with associated neurological and psychological emanation owing to disparity of excitatory and inhibitory neurotransmission. The current study encompasses the assessment of the Nyctanthes arbor-tristis L. methanolic extract (Na.Cr) in the management of convulsive state and concomitant conditions owing to epilepsy. The latency of seizure incidence was assessed using pentylenetetrazol (PTZ) kindling models along with EEG in Na.Cr pretreated mice, trailed by behavior assessment (anxiety and memory), biochemical assay, histopathological alterations, chemical profiling through GCMS, and molecular docking. The chronic assessment of PTZ-induced kindled mice depicted salvation in a dose-related pattern and outcomes were noticeable with extract at 400 mg/kg. The extract at 400 mg/kg defends the progress of kindling seizures and associated EEG. Co-morbid conditions in mice emanating owing to epileptic outbreaks were validated by behavioral testing and the outcome depicted a noticeable defense related to anxiety (P<0.001) and cognitive deficit (P<0.001) at 400 mg/kg. The isolated brains were evaluated for oxidative stress and the outcome demonstrated a noticeable effect in a dose-dependent pattern. Treatment with Na.Cr. also preserved the brain from PTZ induced neuronal damage as indicated by histopathological analysis. Furthermore, the GCMS outcome predicted 28 compounds abundantly found in the plant. The results congregated in the current experiments deliver valued evidence about the defensive response apportioned by Na.Cr which might be due to decline in oxidative stress, AChE level, and GABAergic modulation. These activities may contribute to fundamental pharmacology and elucidate some mechanisms behind the activities of Nyctanthes arbor-tristis. [Display omitted] • Nyctanthes arbor-tristis (NAT) is traditionally used as an antiseizure herb. • We demonstrated the antiseizure potential of NAT extract in PTZ-kindled mice. • EEG and histopathology results showed antiseizure and neuroprotective effects of NAT. • Treatment with NAT also ameliorated anxiety and improved learning and memory. • GC-MS analysis revealed potential 28 key phytoconstituents in NAT. [ABSTRACT FROM AUTHOR]

Chemical kindling is broadly used experimental model to investigate novel treatments on the process of epileptogenesis and coexisting behavioral comorbidities. The current study aimed to investigate the low dose perampanel (PER) (0.125 and 0.5 mg/kg) and pregabalin (PG) (15 mg/kg) as standalone treatments and in combination on kindling-induced seizure progression with concurrent electroencephalographic alterations. Mice were subjected to pentylenetetrazole (PTZ)-induced kindling followed by neurobehavioral assessment for anxiety-like activity and cognitive deficit through behavioral experiments. The monotherapy with PER at 0.5 mg/kg and PG at 15 mg/kg delayed the kindling process but PRP+PG yielded pronounced benefits and hindered the development of seizures of higher severity. PER+PG combination relieved the animals from anxiety-like behavior in various employed anxiogenic tests. Furthermore, the kindling-associated cognitive deficit was protected by PER+PG combination as increased alteration behavior, discrimination index and latencies to enter the dark zone were noted in y-maze, object recognition and passive avoidance tests, respectively while shorter escape latencies were noted in water maze. The brain samples of kindled mice had elevated malondialdehyde and reduced catalase, superoxide dismutase and glutathione peroxidase enzymes while treatment with PER and PG combination shielded the mice from heightened kindling-associated oxidative stress. Overall, the findings of the present study illustrate that concurrent administration of PER and PG effectively hindered the process of epileptogenesis by protecting neuronal excitability and brain oxidative stress. The results predict the dominance of PER and PG combination over monotherapy which might serve as an effective novel combination to combat drug resistance and behavioral disorders in epileptic patients. [Display omitted] • Impact of low doses of perampanel and pregabalin was evaluated in PTZ-kindled mice. • Polypharmacy prevented seizure progression and electrographic changes more effectively. • Combination protected from kindling-associated anxiety, cognitive deficit and depression. • Permapanel and pregabalin protected from kindling-induced brain oxidative stress. [ABSTRACT FROM AUTHOR]

Tiagabine (Tia), a new-generation antiseizure drug that mimics the GABAergic signaling by inhibiting GABA transporter type-1, is the least studied molecule in chronic epilepsy models with comorbid neurobehavioral and neuroinflammatory parameters. Therefore, the current study investigated the effects of Tia in a real-time manner on electroencephalographic (EEG) activity, behavioral manifestations and mRNA expression in pentylenetetrazole (PTZ)-kindled mice. Male BALB/c mice were treated with tiagabine (0.5, 1 and 2 mg/kg) for 21 days with simultaneous PTZ (40 mg/kg) injection every other day for a total of 11 injections and monitored for seizure progression with synchronized validation through EEG recordings from cortical electrodes. The post-kindling protection from anxiety and memory deficit was verified by a battery of behavioral experiments. Isolated brains were evaluated for oxidative alterations and real-time changes in mRNA expression for BDNF/TrkB, GAT-1 and GAT-3 as well as neuroinflammatory markers. Experimental results revealed that Tia at the dose of 2 mg/kg maximally inhibited the development of full bloom seizure and reduced epileptic spike discharges from the cortex. Furthermore, Tia dose-dependently exerted the anxiolytic effects and protected from PTZ-evoked cognitive impairment. Tia reduced lipid peroxidation and increased superoxide dismutase and glutathione levels in the brain via augmentation of GABAergic modulation. PTZ-induced upregulated BDNF/TrkB signaling and pro-inflammatory cytokines were mitigated by Tia with upregulation of GAT-1 and GAT-3 transporters in whole brains. In conclusion, the observed effects of Tia might have resulted from reduced oxidative stress, BDNF/TrkB modulation and mitigated neuroinflammatory markers expression leading to reduced epileptogenesis and improved epilepsy-related neuropsychiatric effects. [Display omitted] • Effect of tiagabine was evaluated during the PTZ-kindling process in mice. • Tiagabine reduced the frequency and amplitude of epileptic spikes in EEG. • Tiagabine improved neurological parameters related to anxiety and memory. • Tiagabine protected against PTZ-induced brain oxidative stress. • The BDNF/TrkB signaling and inflammatory mediators were downregulated by tiagabine. [ABSTRACT FROM AUTHOR]