5,6,7 trihydroxy flavone armoured neurodegeneration caused by Quinolinic acid induced huntington's like disease in rat striatum - reinstating the level of brain neurotrophins with special reference to cognitive-socio behaviour, biochemical and histopathological aspects.

Huntington Disease (HD), a predominant Neurodegenerative Disorder which might be induced by endogenous neurotoxin called Quinolinic Acid (QA), an N-methyl-D aspartate receptor (NMDAR) agonist, the bilaterally intrastriatal administration (200 nm/2 µL of saline) offers rise to the toxic events like neuronal death, neuroinflammation by inflicting excitotoxicity and oxidative stress in the striatum of male Wistar rats by exhibiting the behavioural changes which was accessed by rotarod, open field analysis. In this study, the neuropharmacological effect of Baicalein (BC) against QA induced HD was evaluated. Baicalein (BC), scientifically 5,6,7 trihydroxy flavone present naturally in the edible plants like Scutellaria baicalensis and Oroxylum indicum possess a better neuroprotective effect in the dosage of 10 mg/kg and 30 mg/kg intraperitoneally in the striatum of HD induced rats. This study proved that BC is efficient to revive the level of enzymatic & non-enzymatic antioxidants and mitochondrial complexes by decreasing the number of inflammatory mediators such as MDA, protein carbonyls and Nitric Oxide at the significance of P < 0.01 and restores the amount of BDNF and GDNF thereby preventing the neurophysiological changes which were analysed by haematoxylin & eosin staining. Thus finally, the protective effect of Baicalein displays the up-gradation of psychological and behavioural changes induced by QA.

Extenuation of in utero toxic effects of MeHg in the developing neurons by Fisetin via modulating the expression of synaptic transmission and plasticity regulators in hippocampus of the rat offspring.

The neurotoxic environmental contaminant, methylmercury (MeHg), has shown to have detrimental effects on the developing brain when exposed during gestation. We have shown in our earlier studies that gestational administration of 3,3',4',7-Tetrahydroxyflavone or Fisetin reduces the toxic effects of MeHg in the developing rat brain. The current study has pivoted to study the mechanism behind the mitigating action of Fisetin against prenatal MeHg exposure induced neurotoxicity. Negligible data is available about the toxicity targets of MeHg in the developing brain. Studies have exhibited that MeHg exposure cause toxic effects on synaptic transmission and plasticity in the offspring brain. Hence, we aimed to study the effect of Fisetin on MeHg induced alterations in the expressions of regulatory genes and proteins involved in synaptic plasticity and transmission. Pregnant rats were grouped according to the type of oral administration as, (i) Control, (ii) MeHg (1.5 mg/kg b. w.), (iii) MeHg + Fisetin (30 mg/kg b. w.) and (iv) Fisetin (30 mg/kg b. w). Maternal administration of Fisetin prevented MeHg exposure induced downregulation of neurogranin (Nrgn), dendrin (Ddn), Syntaxin 1 A (Stx1a), Lin-7 homolog A (Lin7a), Complexin-2 (Cplx2) and Exocyst complex component 8 (Exoc8) genes in the offspring rat. Fisetin also prevented MeHg exposure induced downregulation of brain derived neurotrophic factor (BDNF), Glial-cell derived neurotrophic factor (GDNF) protein expressions and hampered reactive astrogliosis in the hippocampus of F1 generation rats. Hence, through this study, we conclude that Fisetin modulates the expression of regulatory genes and proteins involved in synaptic transmission and plasticity and extenuates MeHg neurotoxicity in the developing rat brain.

Hinokitiol Offers Neuroprotection Against 6-OHDA-Induced Toxicity in SH-SY5Y Neuroblastoma Cells by Downregulating mRNA Expression of MAO/α-Synuclein/LRRK2/PARK7/PINK1/PTEN Genes.

Parkinson's disease (PD) remarks its pathology by affecting the patient's movements and postural instability by dopaminergic loss in the substantia nigra of midbrain. The disease is characterized by the accumulation of alpha-synuclein protein followed by dementia symptoms. Moreover, the pathology enhances the production of monoamine oxidases A and B (MAO A and B), leucine-rich repeat kinase 2 (LRRK2), phosphate and tensin homolog (PTEN), PTEN-induced putative kinase 1 (PINK1), and PARK7 (deglycase 1 (DJ-1)). Hinokitiol (HIN), a tropolone-related compound, has widely been reported as an antioxidant, antineuralgic as well as a neuroprotective agent. Hence, in this study, we have examined the effect of hinokitol to act as a neuroprotective agent against 6-OHDA-induced toxicity in SH-SY5Y neuroblastoma cells through downregulation of the mRNA expression of PD pathological proteins like alpha-synuclein, MAO A and B, LRRK2, PTEN, PINK1, and PARK7 (deglycase 1 (DJ-1)). The study revealed that the 6-OHDA-induced elevation in the mRNA expression of the pathology marker proteins was subsequently downregulated by the treatment with HIN and was referenced with the positive control, amantadine (AMA), widely used nowadays as a treatment drug for PD symptoms. Thus, the study suggests that hinokitiol could be a drug of choice against 6-OHDA-induced neurotoxicity in SH-SY5Y neuroblastoma cells.

Quinolinic Acid-Induced Huntington Disease-Like Symptoms Mitigated by Potent Free Radical Scavenger Edaravone-a Pilot Study on Neurobehavioral, Biochemical, and Histological Approach in Male Wistar Rats.

In this study, we demonstrated for the first time the neuroprotective role of edaravone (Eda) (5 and 10 mg/kg b.w.), a potent free radical scavenger against the unilateral stereotaxic induction of quinolinic acid (QA) (300 nm/4 µl saline)-induced Huntington disease (HD)-like symptoms in behavioral, biochemical, and histological features in male Wistar rats striatum. QA induction, which mimics the early stage of HD, commonly causes oxidative stress to the cell and decreases the antioxidant defense mechanism by altering the level of lipid peroxidation (LPO), protein carbonyls, and nitrate concentration (NO) and the activities of glutathione family enzymes (GPx, GST, GR) and acetyl choline esterase concentration (AChE) which was found to be ameliorated by Eda treatment in both the tested doses 5 and 10 mg/kg b.w. in the significance of P < 0.05 and P < 0.01, respectively. Finally histopathological analysis by hematoxylin and eosin stain concluded the promising neurodefensive role of Eda in rat striatum at the dosage of 10 mg/kg b.w., with the decreased tissue damage and the number of damaged granular cells when compared to QA-induced groups.

Methylmercury exposure develops atherosclerotic risk factors in the aorta and programmed cell death in the cerebellum: ameliorative action of Celastrus paniculatus ethanolic extract in male Wistar rats.

Methylmercury (MeHg) is a bioaccumulative global environmental contaminant present in fishes and seafood. MeHg is the methylated form of mercury emitted from diverse anthropogenic and natural sources. MeHg is accumulated in the aquatic environment and eventually reaches human system via food chain by biomagnification. We have reported previously that the neurotoxic effect of MeHg in rat cerebellum is mitigated by the administration of an ayurvedic medicinal plant, Celastrus paniculatus ethanolic extract. The present study has focussed to further explore the mechanism of action of Celastrus paniculatus against MeHg-induced neurotoxicity in the cerebellum. We have also inspected the effect of Celastrus paniculatus (CP) against MeHg-induced atherosclerotic risk factors like alterations in antioxidant levels, aortic lipid profile, and aortic histology by MeHg in the largest vasculature, aorta, which are the initiating factors of cardiovascular diseases. Male Wistar rats were divided as (i) control, (ii) MeHg (5 mg/kg b.w.), (iii) MeHg + CP (200 mg/kg b.w.), and (iv) CP alone (200 mg/kg b.w.). All were given orally for 21 days. In cerebellum Celastrus paniculatus, there were increased mitochondrial electron transport chain (p < 0.05) activity, reduced cytochrome c release (p < 0.05), and caspase 3 mRNA expression (p < 0.05). In the aorta, MeHg-induced oxidative stress, lipid profile changes, and endothelial denudation were ameliorated by Celastrus paniculatus. Hence, we conclude that Celastrus paniculatus protects against MeHg toxicity by inhibiting mitochondrial cytochrome c/caspase 3 apoptotic pathway in the cerebellum and reducing the development of atherosclerotic risk factors in the aorta.

Protective role of apigenin on rotenone induced rat model of Parkinson's disease: Suppression of neuroinflammation and oxidative stress mediated apoptosis.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra which is associated with oxidative stress, neuroinflammation and apoptosis. Apigenin (AGN), a non-mutagenic flavone found in fruits and vegetables, exhibits a variety of biological effects including anti-apoptotic, anti-inflammatory, and free radical scavenging activities. The current study was aimed to investigate the neuroprotective effects and molecular mechanisms of AGN in a rat model of PD induced by rotenone (ROT). Unilateral stereotaxic intranigral infusion of ROT caused the loss of tyrosine hydroxylase (TH) immunoreactivity in striatum and substantia nigra. AGN treatment (10 and 20 mg/kg, i.p.) showed a significant improvement in behavioral, biochemical and mitochondrial enzyme activities as compared to ROT exposed rats. The mRNA expression of inflammatory markers and neurotrophic factors was quantified by reverse transcriptase polymerase chain reaction (RT-PCR). Administration of AGN significantly attenuated the upregulation of NF-κB gene expression in ROT induced group and prevented the neuroinflammation in substantia nigra pars compacta (SNpc). Further, AGN inhibited the release of pro-inflammatory cytokines TNF- α, IL-6 and pro-inflammatory enzyme iNOS-1 induced by ROT. Additionally, AGN prevents the reduction of neurotrophic factors BDNF and GDNF mRNA expression in ROT lesioned rats. Immunoblot results illustrated that AGN treatment downregulated α-synuclein aggregation and upregulated the TH protein expression as well as dopamine D2 receptor (D2R) expression in ROT lesioned rats. Thus, the present findings collectively suggest that AGN exerts its neuroprotection in ROT model of PD and may act as an effective agent for treatment of PD.

Effect of rutin against a mitochondrial toxin, 3-nitropropionicacid induced biochemical, behavioral and histological alterations-a pilot study on Huntington's disease model in rats.

Dietary compounds like flavonoids may offer protection against neurodegeneration. Huntington's disease (HD) is a neurodegenerative disorder characterized by symptoms like chorea and dementia. 3-Nitropropionic acid (3-NP), a Succinate dehydrogenase (SDH) inhibitor produces behavioral, biochemical and histological changes in the striatum, mimics HD in animals and humans. The present study was designed to examine the protective activity of Rutin (RT), a primary flavonoid from citrus fruits, green tea on 3-NP induced experimental model of HD in rats. Rats were pretreated with Rutin, a potent antioxidant (25 and 50 mg/kg b.w.) orally prior to the intraperitoneally (i.p.) administration of 3-NP (10 mg/kg b.w.) for 14 days. Behavioral assessments were carried out on 5th, 10th and 15th day after 3-NP treatment. Body weight, biochemical and histological studies were analyzed on 15th day. Systemic administration of 3-NP significantly reduced the body weight, locomotor activities (Rota rod, Open field test), memory (Morris water maze) and antioxidants such as Glutathione (GSH) levels, activities of Superoxide dismutase (SOD), Catalase (CAT), Glutathione peroxidase (GPx), Glutathione-S-transferase (GST), Glutathione reductase (GR). 3-NP also produces striatal damage by increased the levels of lipid peroxides, nitrite, Glial Fibrillary Acidic Protein (GFAP) and activity of Acetylcholine esterase (AchE). Thus, Rutin treatment of 25 and 50 mg/kg b.w. has significantly restored all the biochemical, behavioral and histological alterations caused by the 3-NP through its antioxidant activity. The findings of our study indicates that Rutin may have an important role in protecting the striatum from oxidative/nitrosative insults caused by 3-NP. These results suggest that RT might be a drug of choice to treat HD.

L-Theanine alleviates the neuropathological changes induced by PCB (Aroclor 1254) via inhibiting upregulation of inflammatory cytokines and oxidative stress in rat brain.

The present study is aimed at evaluating the protective role of L-theanine on aroclor 1254-induced oxidative stress in rat brain. Intraperitoneal administration of Aroclor 1254 (2 mg/kg b.wt. for 30 days) caused oxidative stress in rat brain and also caused neurobehavioral changes. Oxidative stress was assessed by determining the levels of lipid peroxide (LPO), protein carbonyl content, and changes in activities of creatine kinase (CK), acetylcholinesterase (AchE), and ATPases in the hippocampus, cerebellum and cerebral cortex of control and experimental rats. Histopathological results showed that PCB caused neuronal loss in all three regions. PCB upregulated the mRNA expressions of inflammatory cytokines. Oral administration of L-theanine (200 mg/kg b.wt.) increased the status of antioxidants, decreased the levels of LPO, nitric oxide (NO) and increased the activities of CK, AchE and ATPases. L-Theanine restored normal architecture of brain regions and downregulated the expression of inflammatory cytokines. In conclusion, L-theanine shows a protective role against PCBs-induced oxidative damage in rat brain.

Neuroprotective Effect of Portulaca oleraceae Ethanolic Extract Ameliorates Methylmercury Induced Cognitive Dysfunction and Oxidative Stress in Cerebellum and Cortex of Rat Brain.

Methylmercury (MeHg) is highly toxic, and its principal target tissue in human is the nervous system, which has made MeHg intoxication a public health concern for many decades. Portulaca oleraceae (purslane), a member of the Portulacaceae family, is widespread as a weed and has been ranked the eighth most common plant in the world. In this study, we sought for potential beneficial effects of Portulaca oleracea ethanolic extract (POEE) against the neurotoxicity induced by MeHg in cerebellum and cortex of rats. Male Wistar rats were administered with MeHg orally at a dose of 5 mg/kg b.w. for 21 days. Experimental rats were given MeHg and also administered with POEE (4 mg/kg, orally) 1 h prior to the administration of MeHg for 21 days. After MeHg exposure, we determine the mercury concentration by atomic absorption spectroscopy (AAS); mercury content was observed high in MeHg-induced group. POEE reduced the mercury content. We also observed that the activities of catalase, superoxide dismutase, glutathione peroxidase, and the level of glutathione were reduced. The levels of glutathione reductase and thiobarbituric acid reactive substance were found to be increased. The above biochemical changes were found to be reversed with POEE. Behavioral changes like decrease tail flick response, longer immobility time, and decreased motor activity were noted down during MeHg exposure. POEE pretreatment offered protection from these behavioral changes. MeHg intoxication also caused histopathological changes in cerebellum and cortex, which was found to be normalized by treatment with POEE. The present results indicate that POEE has protective effect against MeHg-induced neurotoxicity.

Protective effect of L-Theanine against aluminium induced neurotoxicity in cerebral cortex, hippocampus and cerebellum of rat brain - histopathological, and biochemical approach.

L-Theanine is an amino acid derivative primarily found in tea. It has been reported to promote relaxation and have neuroprotective effects. The present study was designed to investigate the role of oxidative stress and the status of antioxidant system in the management of aluminum chloride (AlCl3) induced brain toxicity in various rat brain regions and further to elucidate the potential role of L-Theanine in alleviating such negative effects. Aluminium administration significantly decreased the level of reduced glutathione and the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, Na(+)/K(+) ATPase, Ca(2+) ATPase and Mg(2+) ATPase and increased the level of lipid peroxidation and the activities of alkaline phosphatase, acid phosphatase, alanine transaminase and aspartate transaminase in all the brain regions when compared with control rats. Pre-treatment with L-Theanine at a dose of 200 mg/kg b.w. significantly increased the antioxidant status and activities of membrane bound enzymes and also decreased the level of LPO and the activities of marker enzymes, when compared with aluminium induced rats. Aluminium induction also caused histopathological changes in the cerebral cortex, cerebellum and hippocampus of rat brain which was reverted by pretreatment with L-Theanine. The present study clearly indicates the potential of L-Theanine in counteracting the damage inflicted by aluminium on rat brain regions.

Nephroprotective potential of Bacopa monniera on hypercholesterolemia induced nephropathy via the NO signaling pathway.

CONTEXT: Bacopa monniera L. (Scrophulariaceae) is used as a traditional medicine in India for various ailments such as epilepsy, mental disorders, and also as a cardio-tonic. However, its nephroprotective role is still unknown. OBJECTIVE: The present study assesses the modulatory impact of the alcoholic (ethanol) extract of Bacopa monniera (AEBM) on renal oxido-lipidemic stress in hypercholesterolemic rats. MATERIALS AND METHODS: B. monniera (1 kg) was extracted with 90% ethanol, filtered, and dried (52 g). Group-I rats as control, Group-II rats fed with a hypercholesterolemic diet (HCD) for 45 d [4% cholesterol and 1% cholic acid], Group-III rats fed with HCD for 45 d + AEBM (40 mg/kg, body weight) for last 30 d, and Group-IV AEBM alone rats. Blood and kidney were removed to analyze lipid, antioxidant status, and histological analysis. RESULT: The levels of total cholesterol (TC), triacylglycerol (TG), phospholipids (PLs), renal functional parameters (urea, creatinine, and uric acid), and lipid peroxidation (LPO) products were significantly attenuated (p < 0.01) in AEBM-treated hypercholesterolemic rats. Activities of both enzymic (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and glutathione reductase (GR)) and non-enzymic antioxidant (GSH, Vit-C, and Vit-E) were significantly increased (p < 0.01), on supplementation with AEBM. Administration with AEBM the mRNA levels of eNOS and iNOS genes was significantly up-regulated and down-regulated (p < 0.01). Histomorphological observations also evidenced that AEBM effectively protects the kidney from hypercholesterolemia-mediated oxido-lipidemic damage. DISCUSSION AND CONCLUSION: From this study, we hypothesized that AEBM can act as renoprotective agent by attenuating the renal oxido-lipidemic stress via regulating NOS level and thereby protects the nephron in hypercholesterolemic rats.

Effect of Bacopa monniera extract on methylmercury-induced behavioral and histopathological changes in rats.

Methylmercury (MeHg) is a well-recognized environmental contaminant with established health risk to human beings by fish and marine mammal consumption. Bacopa monniera (BM) is a perennial herb and is used as a nerve tonic in Ayurveda, a traditional medicine system in India. This study was aimed to evaluate the effect of B. monniera extract (BME) on MeHg-induced toxicity in rat cerebellum. Male Wistar rats were administered with MeHg orally at a dose of 5 mg/kg b.w. for 21 days. Experimental rats were given MeHg and also administered with BME (40 mg/kg, orally) 1 h prior to the administration of MeHg for 21 days. After treatment period, MeHg exposure significantly decreases the body weight and also caused the following behavioral changes. Decrease tail flick response, longer immobility time, significant decrease in motor activity, and spatial short-term memory. BME pretreatment reverted the behavioral changes to normal. MeHg exposure decreases the DNA and RNA content in cerebellum and also caused some pathological changes in cerebellum. Pretreatment with BME restored all the changes to near normal. These findings suggest that BME has a potent efficacy to alleviate MeHg-induced toxicity in rat cerebellum.

Antihypercholesterolemic effect of Bacopa monniera linn. on high cholesterol diet induced hypercholesterolemia in rats.

OBJECTIVE: To explore the effect of alcoholic extract of Bacopa monniera (AEBM) on high cholesterol diet-induced rats. METHODS: The shade-dried and coarsely powdered whole plant material (Bacopa monniera) was extracted with 90% ethanol, finally filtered and dried in vacuum pump. The experimental rats were divided into 4 groups: control (group-I), Rats fed with hypercholesterolemic diet (HCD) for 45 days [4% cholesterol (w/w) and 1% cholic acid], Rats fed with HCD for 45 days+AEBM (40mg/kg, body weight/day orally) for last 30 days (group-III) and AEBM alone (group-IV). Blood and tissues (Aorta) were removed to ice cold containers for various biochemical and histological analysis. RESULTS: AEBM treatment significantly decreased the levels of TC, TG, PL, LDL, VLDL, atherogenic index, LDL/HDL ratio, and TC/HDL ratio but significantly increased the level of HDL when compared to HCD induced rats. Activities on liver antioxidant status (SOD, CAT, GPx, GR, GST) were significantly raised with concomitant reduction in the level of LPO were obtained in AEBM treated rats when compared to HCD rats. Treatment with AEBM significantly lowered the activity of SGOT, LDH and CPK. Histopathology of aorta of cholesterol fed rat showed intimal thickening and foam cell deposition were noted. CONCLUSIONS: These results suggests that AEBM extended protection against various biochemical changes and aortic pathology in hypercholesterolemic rats. Thus the plant may therefore be useful for therapeutic treatment of clinical conditions associated hypercholesterolemia.

Alcoholic extract of Bacopa monniera Linn. protects against 6-hydroxydopamine-induced changes in behavioral and biochemical aspects: a pilot study.

Parkinson's disease is one of the commonest neurodegenerative diseases, and oxidative stress has been evidenced to play a vital role in its causation. In this study, we evaluated whether alcoholic extract of Bacopa monniera (AEBM), an antioxidant and memory enhancer can slow the neuronal injury in a 6-OHDA-rat model of Parkinson's. Rats were treated with 20 and 40 mg/kg bodyweight of AEBM for 3 weeks. On Day 21, 2 µl of 6-OHDA (12 µg in 0.01 % in ascorbic acid-saline) was infused into the right striatum, while the control group received 2 µl of vehicle. Three weeks after the 6-OHDA injection, the rats were tested for neurobehavioral activity (rotarod, locomotor activity, grip test, forced swim test, radial arm maze) and were killed after 6 weeks for the estimation of lipid peroxidation, reduced glutathione (GSH) content, activities of glutathione-S-transferase, glutathione reductase, glutathione peroxidase, superoxide dismutase (SOD), and catalase (CAT). The deficits in behavioral activity due to 6-OHDA lesioning were significantly and dose dependently restored by AEBM. Lesioning was followed by an increased lipid peroxidation and significant depletion of reduced GSH content in the substantia nigra, which was prevented with AEBM pretreatment. The activities of GSH-dependent enzymes, CAT and SOD in striatum were reduced significantly by lesioning, which were restored significantly and dose dependently by AEBM. This study indicates that the extract of B. monniera might be helpful in attenuating 6-OHDA-induced lesioning in rats.

Protective effect of Bacopa monniera on methyl mercury-induced oxidative stress in cerebellum of rats.

Methyl mercury (MeHg) is a ubiquitous environmental pollutant leading to neurological and developmental deficits in animals and human beings. Bacopa monniera (BM) is a perennial herb and is used as a nerve tonic in Ayurveda, a traditional medicine system in India. The objective of the present study was to investigate whether Bacopa monniera extract (BME) could potentially inhibit MeHg-induced toxicity in the cerebellum of rat brain. Male Wistar rats were administered with MeHg orally at a dose of 5 mg/kg b.w. for 21 days. Experimental rats were given MeHg and also administered with BME (40 mg/kg, orally) for 21 days. After the treatment period, we observed that MeHg exposure significantly inhibited the activities of superoxide dismutase, catalase, glutathione peroxidase, and increased the glutathione reductase activity in cerebellum. It was also found that the level of thiobarbituric acid-reactive substances was increased with the concomitant decrease in the glutathione level in MeHg-induced rats. These alterations were prevented by the administration of BME. Behavioral interference in the MeHg-exposed animals was evident through a marked deficit in the motor performance in the rotarod task, which was completely recovered to control the levels by BME administration. The total mercury content in the cerebellum of MeHg-induced rats was also increased which was measured by atomic absorption spectrometry. The levels of NO(2) (-) and NO(3) (-) in the serum were found to be significantly increased in the MeHg-induced rats, whereas treatment with BME significantly decreased their levels in serum to near normal when compared to MeHg-induced rats. These findings strongly implicate that BM has potential to protect brain from oxidative damage resulting from MeHg-induced neurotoxicity in rat.

Protective role of Cynodon dactylon in ameliorating the aluminium-induced neurotoxicity in rat brain regions.

Cynodon dactylon (Poaceae) is a creeping grass used as a traditional ayurvedic medicine in India. Aluminium-induced neurotoxicity is well known and different salts of aluminium have been reported to accelerate damage to biomolecules like lipids, proteins and nucleic acids. The objective of the present study was to investigate whether the aqueous extract of C. dactylon (AECD) could potentially prevent aluminium-induced neurotoxicity in the cerebral cortex, hippocampus and cerebellum of the rat brain. Male albino rats were administered with AlCl(3) at a dose of 4.2 mg/kg/day i.p. for 4 weeks. Experimental rats were given C. dactylon extract in two different doses of 300 mg and 750 mg/keg/day orally 1 h prior to the AlCl(3) administration for 4 weeks. At the end of the experiments, antioxidant status and activities of ATPases in cerebral cortex, hippocampus and cerebellum of rat brain were measured. Aluminium administration significantly decreased the level of GSH and the activities of SOD, GPx, GST, Na(+)/K(+) ATPase, and Mg(2+) ATPase and increased the level of lipid peroxidation (LPO) in all the brain regions when compared with control rats. Pre-treatment with AECD at a dose of 750 mg/kg b.w increased the antioxidant status and activities of membrane-bound enzymes (Na(+)/K(+) ATPase and Mg(2+) ATPase) and also decreased the level of LPO significantly, when compared with aluminium-induced rats. The results of this study indicated that AECD has potential to protect the various brain regions from aluminium-induced neurotoxicity.

Alcoholic extract of 'Bacopa monniera' reduces the in vitro effects of morphine withdrawal in guinea-pig ileum.

The effect of the alcoholic extract of the whole plant of Bacopa monniera (Scrophulariaceae) on morphine withdrawal was evaluated in vitro in guinea-pig ileum. After a 4 min in vitro exposure to morphine, addition of naloxone induced a strong contraction. Addition of various concentrations of the alcoholic extract of B. monniera (100-1000 microg/ml) 15 min before exposure to morphine reduced the naloxone-induced contraction in a dose-dependent manner. The results suggest that B. monniera extract may be useful in reducing the withdrawal symptoms induced by morphine.