Protective effects of Pluchea lanceolata on dementia induced by omeprazole in experimental rats (original) (raw)
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The beneficial effect of Pluchea lanceolata on aluminum chloride-induced Alzheimer's disease in rats
Journal of Cellular Neuroscience and Oxidative Stress
Aluminum chloride (AlCl3) causes neuroinflammation in rats, which leads to the development of Alzheimer's disease. The current study focused on the anti-Alzheimer and antioxidant potential of hydromethanolic extracts of Pluchea lanceolata (PL), a well-known Rasna source. Phytoconstituents such as pluchine and moretenol acetate are selected for the PASS online and molecular docking (in silico) experimental model. A total of 36 Wistar rats were divided into VI groups, each with six rats. Group I: normal control, Group II: disease control, Group III: Rivastigmine (0.3 mg/kg, p.o), Group IV and V: Hydromethanolic extract of PL (HMEPL, 200 mg/kg, 400 mg/kg, p.o), and Group VI: Ayurvedic Formulation of Rasna (AFR) (1ml/kg, p.o). Except for group I, all of the animals were given Aluminum Chloride (AlCl3) (300 mg/kg, p.o). AlCl3 and plant extracts were given for 20day treatment. On the 0th, 7th, 14th, and 20th days, the behavioural study and changes in body weight were evaluated. Rats w...
PLoS ONE, 2013
The present study investigates the potential of lansoprazole (a proton pump inhibitor and agonist of liver x receptors) in experimental dementia of AD type. Streptozotocin [STZ, 3 mg/kg, injected intracerebroventricular (i.c.v), and high fat diet (HFD, administered for 90 days)] were used to induce dementia in separate groups of Swiss mice. Morris water maze (MWM) test was performed to assess learning and memory of the animals. A battery of biochemical and histopathological studies were also performed. Extent of oxidative stress was measured by estimating the levels of brain reduced glutathione (GSH) and thiobarbituric acid reactive species (TBARS). Brain acetylcholinestrase (AChE) activity and serum cholesterol levels were also estimated. The brain level of myeloperoxidase (MPO) was measured as a marker of inflammation. STZ and HFD produced a marked decline in MWM performance of the animals, reflecting impairment of learning and memory. STZ/HFD treated mice exhibited a marked accentuation of AChE activity, TBARS and MPO levels along with a fall in GSH levels. Further, the stained micrographs of STZ/HFD treated mice indicated pathological changes, severe neutrophilic infiltration and amyloid deposition. Lansoprazole treatment significantly attenuated STZ and HFD-induced memory deficits, biochemical and histopathological alterations. It also prevented HFD-induced rise in the cholesterol level. Therefore, the findings demonstrate potential of lansoprazole in memory dysfunctions which may probably be attributed to its anticholinesterase, anti-oxidative and anti-inflammatory effects. Moreover, both cholesterol-dependent as well as cholesterolindependent effects of lansoprazole appear to play a role. In addition study indicates the role of liver x receptors in dementia.
Effect of Pluchea lanceolata bioactives in LPS-induced neuroinflammation in C6 rat glial cells
Naunyn-Schmiedeberg's Archives of Pharmacology, 2014
Neuroinflammation plays a significant role in various chronic and acute pathological conditions of the central nervous system. In the Indian system of medicine, Pluchea lanceolata is used to treat the neurological disorders. We investigated the effect of major pentacyclic triterpene and its naturally occurring acetate derivative isolated from P. lanceolata on lipopolysaccharide (LPS)-stimulated neuroinflammatory condition associated to inflammatory cytokine production in rat astrocytoma cell line (C6). The log concentration dependence of Pluchea bioactive taraxasterol (Tx) significantly (p <0.05) attenuates the release of proinflammatory cytokines, such as TNF-α, IFN-γ, and IL-6, while its in situ produced acetyl derivative, i.e., taraxasterol acetate (TxAc), did not inhibit the LPS-induced IL-6 production at lower concentration (p >0.05). Surflex-Dock molecular modeling study was performed to simulate the binding capacity of compounds into the active site of the TNF-α (2AZ5), tumor protein P53 (2VUK), and NF-kappa-B (1RAM). The differential inhibition of cytokines by Tx and TxAc was further confirmed by high docking scores showing the high affinity to target proteins. Findings of the study demonstrated the comparatively greater role of Pluchea triterpene than its in situ produced acetate derivate in neuroinflammation-associated disorders.
Environmental Science and Pollution Research, 2020
The extensive uses of organophosphates and pyrethroids have made it necessary to investigate the neurotoxicity of their combination as they may implicate in the neurodegenerative syndromes. Monoamine oxidase-A (MAO-A) and acetylcholinesterase (AChE) gene expression in the rat brain were evaluated after independent and combined intoxications with chlorpyrifos and cypermethrin. Twenty-four mature male rats were equally distributed into four groups. The first one was kept as a control group, whereas the second, third and fourth were orally gavage with chlorpyrifos (16.324 mg/kg), cypermethrin (25.089 mg/kg) and their combination (9.254 mg/kg), respectively, for 4 weeks. As compared to the control group, intoxications with chlorpyrifos and/or cypermethrin revealed significant (P < 0.05) declines in the levels of brain neurotransmitters (dopamine and serotonin) plus the enzymatic activities of MAO-A, AChE and sodium-potassium adenosine triphosphatase. The mRNA genes expression of MAO-A and AChE have also confirmed the enzymatic actions. Moreover, the oxidative injury recorded as the levels of malondialdehyde and nitric oxide markedly increased (P < 0.01), while the total thiol content reduced and the histopathological outcomes have confirmed these impacts. In conclusion, chlorpyrifos and cypermethrin revealed antagonistic inhibitions on the brain MAO-A and AChE gene regulation through neurotransmission deteriorations and oxidative damage, which could describe their contributions in the neuropathological progressions.
Abstract Background: Acetaminophen (APAP)-induced toxicity is a predominant cause of acute hepatic and renal failure. In both humans and rodents toxicity begins with a reactive metabolite that binds to proteins. This leads to mitochondrial dysfunction and nuclear DNA fragmentation resulting in necrotic cell death. Pleurotus ostreatus (an edible oyster mushroom) is well recognized as a flavourful food, as well as a medicinal supplement. In the present study, we evaluated the role of Pleurotus ostreatus in the protection against APAP-induced hepato-renal toxicity. We also explored the mechanism by which Pleurotus ostreatus exerts its effects. Methods: Ninety adult male Swiss albino mice were divided into three groups (30 mice/group). Mice were offered normal diet (control and APAP groups), or diet supplemented with 10% Pleurotus ostreatus (APAP + Pleurotus ostreatus) for 10 days. Mice were either treated with vehicle (control group, single intra-peritoneal injection.), or APAP (APAP and APAP + Pleurotus ostreatus groups, single intra-peritoneal injection, 500 mg/kg), 24 hours after the last meal. Results: APAP increased serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) glutamate dehydrogenase (GDH), creatinine, blood urea nitrogen (BUN), urinary kidney injury molecule-1 (KIM-1), and hepatic and renal malondialdehyde (MDA) content. APAP decreased hepatic and renal glutathione (GSH) content, as well as glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities. Supplementation with Pleurotus ostreatus significantly reduced APAP-induced elevated levels of ALT, AST, GDH, creatinine, BUN, KIM-1and MDA, while GSH level, and GSH-Px and SOD activities were significantly increased. Our findings were further validated by histopathology; treatment with Pleurotus ostreatus significantly decreased APAP-induced cell necrosis in liver and kidney tissues. Conclusions: We report here that the antioxidant effect of Pleurotus ostreatus opposes mitochondrial dysfunction and oxidative stress accompanying APAP over-dose, with subsequent clinically beneficial effects on liver and kidney tissues. Keywords: Pleurotus ostreatus,
Haloperidol- and clozapine-induced oxidative stress in the rat brain
Pharmacology Biochemistry and Behavior, 2004
Oxidative stress has been implicated in reproductive toxicity induced by antipsychotics (APs). This study aims to further investigate the role of AP-induced oxidative stress in reproductive dysfunction. Thirty adult female albino rats were divided into three groups including a control group (n = 10) receiving distilled water, HAL group (n = 10) receiving haloperidol (HAL) (2 mg/kg/day), and CLZ group (n = 10) receiving clozapine (CLZ) (20 mg/kg/day). After 28 days, the rats were anesthetized, blood was withdrawn from their hearts, and ovaries were removed before they were sacrificed. Serum prolactin concentrations were measured. For each rat, one ovary was used for biochemical studies including mitochondrial complexes I and III activities and oxidative stress markers (lipid peroxidation, super oxide dismutase [SOD], catalase [CAT], and reduced glutathione [GSH]). The other ovary was used for histopathological examination and immunohistochemistry staining for p53 and Ki-67. HAL-treated rats showed significantly (p < 0.001) higher serum prolactin concentrations compared with other groups. HAL significantly inhibited complexes I (p < 0.001) and III activities (p < 0.05), while CLZ inhibited only complex I (p < 0.001). Lipid peroxidation was increased by HAL (p < 0.001) and CLZ (p < 0.01). HAL caused significant (p < 0.001) reductions in SOD, CAT, and GSH. CLZ caused a significant decrease in SOD (p < 0.001) and GSH (p < 0.01) with no effect on CAT. Histopathological studies of CLZ-and HAL-treated ovaries showed features suggestive of hyperprolactinemia and oxidative stress. Ki-67-and P53-immunostained sections were suggestive of disruption of cellular proliferation. These findings support the hypothesis that HAL and CLZ induce reproductive dysfunction through mechanisms involving ovarian mitochondrial dysfunction and oxidative stress.
Drug and chemical toxicology, 2017
Medicinal plants, as new drugs, are considered for treatment of insomnia, anxiety, depression, confusion, nausea, and vomiting symptoms. The current study aimed to evaluate the neuroprotective and antiemetic effects of Albizia. julibrissin Durazz. flower extract in the chickens. Emesis was induced by copper sulfate and ipecac (60 and 600 mg/kg, orally, respectively) and the methanolic extract (50, 100, and 200 mg/kg) were injected intraperitoneally (i.p.). Mitochondrial function, lipid peroxidation (LPO), protein carbonyl (PC) content, and catalase activity as biomarkers of oxidative damage were evaluated in the brain mitochondria. All doses of extract showed significant (p < 0.001) antiemetic activity against induced emesis by copper sulfate and ipecac. Brain mitochondria function (by 50, 100, and 200 mg/kg of extract) were increased 48%, 85%, and 90% against emesis induced by ipecac and 32%, 18%, and 24% against emesis induced by copper sulfate, respectively. LPO and PC content...
Indian journal of experimental biology, 2014
Acute dose of organophosphorus pesticide Triazophos (O,O-diethyl O-1-phenyl-1H-1,2,4-triazol-3-yl phosphorothioate; Tz) administered orally affects oxidative stress parameters and the histo-architecture of liver, kidney and brain tissues. The results indicate a dose dependent induction of oxidative stress as evident by increased malondialdehyde level and decreased antioxidant defense including glutathione and superoxide dismutase activity in rat liver, kidney and brain. AChE activity was found significantly decreased in the Tz treated groups as compared to the vehicle control (DMSO) group. Histopathological examination of liver, kidney and brain in Tz treated rats revealed medullary congestion and hydropic degeneration of hepatocytes in liver and medullary congestion in kidney. However, no significant histopathological changes were observed in brain tissues.
Impact of Imidacloprid on the Mitochondrial Function of Wistar Rats' Nervous System
Journal of chemical health risks, 2024
Pesticides are chemicals used to struggle against harmful pests; they could affect any compartment after getting into nature. Most pesticides are made up of only a selective molecule. When compared to bulk materials like powders, plates, and sheets, pesticides have a relatively large specter-to-volume ratio because of their extremely potent chemical makeup. Because of this characteristic, pesticides might have unexpected chemical and physical characteristics because they interact with the molecules in the environment and compartment. The present assessment aims to test the neurotoxicity induced by a pesticide of Imidacloprid at 1.252 mM kg-1 per day in the Wistar rat's brain. After gavage to the rats for 3 months in laboratory conditions of the groups (light/dark; humidity), tests on nervous system enzymes figured that pesticide caused a significant enhancement of inter-mitochondrial metabolites amount (proteins, fats, and carbohydrates) and mitochondrial enzyme activity (GST and SOD); decreased amount of mitochondrial GSH; an enhancement of mit-CAT and mit-GPx activity; a rise in MDA level. Mitochondrial functions of the treated Rat's brains showed a notable rise in mitochondrial swelling and permeability. Rather, there was a statistically significant drop in the amount of oxygen consumed by mitochondrial respiration. All results confirm that the pesticide caused a dose-dependent response.
Journal of Neurochemistry, 1984
In this work, the effect of chronic intraperitoneal administration of chlorpromazine (5 and 10 mg/kg) on the antioxidant enzymes superoxide disrnutase (SOD), catalase (CA), glutathione reductase (GR), and glutathione peroxidase (GP); lipid peroxidation; and lipofuscin accumulation in the brains of rats ages 6, 9, and 12 months was studied. Chlorpromazine increased the activities of SOD, GR, and GP in particulate fraction from cerebrum, cerebellum, and brain stem in a dose-dependent manner. While GR and SOD associated with soluble fraction increased, GP associated with soluble fraction was not affected. CA did not change after chlorpromazine administration in any regions of the brain of rats from all age groups. Chlorpromazine, thus, had a somewhat different action on antioxidant enzymes in different subcellular fractions. Chlorpromazine inhibited lipid peroxidation, both in vivo and in vitro, and it also inhibited accumulation of lipid peroxidation fluorescent products (lipofuscin), which was studied histochemically and biochemically as well. The data indicate that chlorpromazine inhibition of lipid peroxidation and of accumulation of lipofuscin can result from elevation of the activity of brain antioxidant enzymes. Key Words: Antioxidant enzymes-Glutathione peroxidase-Lipid peroxide-Peroxide-Lipofuscin-Chlorpromazine. Roy D. et al. Effects of chlorpromazine on the activities of antioxidant enzymes and lipid peroxidation in the various regions of aging rat brain.