T. Prakash

Antiulcerogenic activity of Terminalia chebula fruit in experimentally induced ulcer in rats

Context: Terminalia chebula Retz. (Combretaceae) is a medium-sized tree that grows in the wild throughout India. T. chebula has been extensively used in Ayurveda, Unani, and homoeopathic medicine. The fruit has been used as a traditional medicine for a household remedy against various human ailments. Traditionally T. chebula is used to cure chronic ulcer, gastritis, and stomach cancers. Objective: The present study is to evaluate the antiulcer effect of hydroalcoholic (70%) extract of Terminalia chebula fruit. Materials and methods: Aspirin, ethanol and cold restraint stress-induced ulcer methods in rats were used for the study. The effects of the extract on gastric secretions, pH, total and free acidity using pylorus ligated methods were also evaluated. Results: Animals pretreated with doses of 200 and 500 mg/kg hydroalcoholic extract showed significant reduction in lesion index, total affected area and percentage of lesion in comparison with control group (P < 0.05 and P < 0.01) in the aspirin, ethanol and cold restraint stress-induced ulcer models. Similarly extracts increased mucus production in aspirin and ethanol-induced ulcer models. At doses of 200 and 500 mg/kg of T. chebula extract showed antisecretory activity in pylorus ligated model, which lead to a reduction in the gastric juice volume, free acidity, total acidity, and significantly increased gastric pH. Discussion and conclusion: These findings indicate that hydroalcoholic extract of the fruit T. chebula displays potential antiulcerogenic activity. This activity thus lends pharmacological credence to the suggested use of the plant as a natural remedy in the treatment or management of ulcer.

Multifaceted effects of aluminium in neurodegenerative diseases: A review

Aluminium (Al) is the most common metal and widely distributed in our environment. Al was first isolated as an element in 1827, and its use began only after 1886. Al is widely used for industrial applications and consumer products. Apart from these it is also used in cooking utensils and in pharmacological agents, including antacids and antiperspirants from which the element usually enters into the human body. Evidence for the neurotoxicity of Al is described in various studies, but still the exact mechanism of Al toxicity is not known. However, the evidence suggests that the Al can potentiate oxidative stress and inflammatory events and finally leads to cell death. Al is considered as a well-established neurotoxin and have a link between the exposure and development of neurodegenerative diseases, including Amyotrophic Lateral Sclerosis (ALS), Alzheimers disease (AD), dementia, Gulf war syndrome and Parkinsonism. Here, we review the detailed possible pathogenesis of Al neurotoxicity. This review summarizes Al induced events likewise oxidative stress, cell mediated toxicity, apoptosis, inflammatory events in the brain, glutamate toxicity, effects on calcium homeostasis, gene expression and Al induced Neurofibrillary tangle (NFT) formation. Apart from these we also discussed animal models that are commonly used for Al induced neurotoxicity and neurodegeneration studies. These models help to find out a better way to treat and prevent the progression in Al induced neurodegenerative diseases.

Reduction in drop size of ophthalmic topical drop preparations and the impact of treatment.

In this work we devised a method to create smaller eye drops of the glaucoma medication timolol maleate by altering the dropper tip design and changing the physical properties of the formulation. Most ocular diseases are treated with topical application of eye drops. After instillation of an eye drop, typically, less than 5% of the applied drug penetrates the cornea and reaches the intraocular tissues; the major fraction of the instilled drug is absorbed and enters the systemic circulation. Ophthalmic solutions are available in multidose or single-dose glass/plastic dropper bottles that deliver drops with a volume that ranges from 25 μL to 70 μL (average 40 μL). Because of the low capacity of the precorneal area, the optimal drop volume is about 20 μL; with larger volumes there is the risk of adverse systemic effects due to absorption of the drug via the nasal mucosa. Thus, both from the biopharmaceutical and economic point of view, drops of only 5-15 mL volume should be instilled into the eye. In this present work we devised a method to reduce the size of the drop by inserting a glass capillary tube into the dropper tip and by changing the physical properties of the formulation (by altering the concentration of Tween 80™, i.e., 0.05% and 0.1% of Tween 80™). We measured the drop sizes of the different timolol eye drop formulations available in the market and estimated the yearly cost of the medications. Our timolol maleate formulation with 0.1% concentration of Tween 80™ delivered through the dropper tip with the inserted glass capillary was shown to be better than the other formulations available in the market in terms of ability to deliver smaller drops, meaning that each bottle would last longer and that the yearly cost of treatment would be lower.

Study on cerebroprotective actions of Clerodendron glandulosumleaves extract against long term bilateral common carotid artery occlusion in rats

Stroke is a major cause of death and disability worldwide. The resulting burden on the society continues to grow, with increase in the incidence of stroke. Oxidative stress has been involved in the pathogenesis of several neurological diseases including acute stroke.Focal and global cerebral ischemia represents diseases that are common in the human population.In recent years much attention is being paid towards the exploration of herbal preparation, antioxidant agents and combination therapies including COX-2 inhibitors in experimental model of stroke.Possible effect of a hydroalcoholic leaf extract of Clerodendron glandulosumColeb (C. glandulosum)on oxidant-antioxidant status in ischemia-hypoperfusion injury in the rat forebrain has been investigated.Healthy adult male Wistar albino rats were divided into five groups (n=8). Group I was served as Sham control (normal saline 1ml/kg, orally), group II was served hypoperfusion control (normal saline 1ml/kg, orally), group III, group IV were served as hydroalcoholic extract treated (200 and 400mg/kg, orally) and group V was treated with Quercetin (10mg/kg, orally) for 14days to assess preventive and curative effects of C. glandulosum. Flavonoid and phenolic compounds exhibit a broad spectrum of biological activity, including antioxidant. C. glandulosum extract (200 and 400mg/kg, p.o) was administered orally, once daily for a period of 2 weeks after the occlusion of BCCA. After 14th days rats were subjected to behavioral studies. After behavioral studies animals were sacrificed and brain was removed and homogenized. Estimation of Lipid peroxidation (LPO) Myeloperoxidase (MPO), estimation of protein levels and the activities of Superoxide dismutase (SOD), Catalase (CAT), were performed. Infarct size and histopathological changes were observed in treated groups.

Synthesis of ZnO Nanostructures by Microwave Irradiation Using Albumen as a Template

ZnO nanostructures have been successfully prepared by a microwave irradiation method. The role of albumen as a template in addressing the size and morphology of ZnO has been investigated by X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FT-IR), thermogravimetric analysis (TG-DTA), scanning electron microscopy (SEM), and transmission electron microscopy (TEM) techniques. A heterogeneous mixture of Zn(OH)2 and ZnO was obtained in absence of albumen. Pure ZnO nanostructures, consisting of rod- and whisker-like nanoparticles embedded in a sheet matrix, were obtained in the presence of albumen. Optical and photoluminescence (PL) properties of the synthesized samples were also compared. Results obtained indicate that the microwave-assisted method is a promising low temperature, cheap, and fast method for the production of ZnO nanostructures.

Protective effect of co-administration of curcumin and sildenafil in alcohol induced neuropathy in rats

&NA; Neuropathic pain associated with chronic alcohol consumption is a medico‐socioeconomical problem that affects both central and peripheral nervous system and has no satisfactory treatment till date. The present study was designed to investigate the protective effect of co‐administration of curcumin and sildenafil on alcohol induced neuropathic pain in rats. In order to carry out this, ethanol (35% v/v, 10 g/kg, p.o.) was administered for 10 weeks to induce neuropathic pain. Curcumin (30 and 60 mg/kg, i.p.) and sildenafil (5 and 10 mg/kg, i.p.) were given alone and in combination at their lower doses (30 mg/kg curcumin and 5 mg/kg, sildenafil, i.p.) to investigate the changes in thermal and mechanical hyperalgesia, allodynia and histopathological parameters. Biochemical estimations of thiobarbituric acid reactive species, glutathione and protein was also carried out to evaluate oxidative stress. The results revealed that chronic alcohol consumption for 10 weeks caused significant thermal and mechanical hyperalgesia, allodynia and increased oxidative stress. Individual administration of both the drugs at their low as well as high doses were able to improve the symptoms of alcohol induced neuropathic pain. Whereas co‐administration of curcumin and sildenafil at their lower doses itself were found to significantly improve nerve functions, biochemical and histopathological parameters as compared to their individual administration. It is therefore proposed that co‐administration of curcumin and sildenafil may bring new dimension towards attenuation of alcohol induced neuropathic pain affecting central as well as peripheral nervous system. Graphical abstract Figure. No caption available.

Preparation of Niobium Metal Powder by Two-Stage Magnesium Vapor Reduction of Niobium Pentoxide

Magnesium vapor reduction of niobium pentoxide was studied using a laboratory system. Niobium powder was prepared by the magnesium vapor reduction at 1123 K for 5 hours and it contained about 8 mass % oxygen. However, the oxygen concentration could be decreased to 0.65% when it was prepared by double-step reduction by magnesium vapor and a chemical treatment. Controlled and diluted supply of magnesium vapor to the reaction front has averted excess heat generation at the reaction front and thereby fine particles were produced. Effects of various factors on the vapor reduction process were studied and discussed.

Effect of wedelolactone and gallic acid on quinolinic acid-induced neurotoxicity and impaired motor function: significance to sporadic amyotrophic lateral sclerosis

HighlightsQuinolinic acid is well known endogenous neuroactive metabolite of tryptophan degradation pathway.Quinolinic acid causes neurotoxicity and impairment in motor function and motor learning memory.Wedelolactone and Gallic acid were improved the motor function and motor learning ability in the rats.Wedelolactone and Gallic acid are capable to act through various pathways and can reduce reverse the toxic events triggered by quinolinic acid. ABSTRACT Quinolinic acid (QUIN) is a well‐known neuroactive metabolite of tryptophan degradation pathway or kynurenine pathway. The QUIN is involved in the development of several toxic cascades which leads to the neuronal degeneration processes. The QUIN‐induced toxicity is also responsible for the impairment of the motor function and motor learning ability. This study seeks to investigate the several mechanisms which are involved in the intrastriatal administration of QUIN‐induced neurodegeneration and the neuroprotective effects of wedelolactone (WL) and gallic acid (GA) over QUIN‐induced toxicity. The Wistar rats were used for the study and conducted behavioral model to evaluate the effects of WL (100 & 200 mg/kg) and GA (100 & 200 mg/kg) on impaired motor function and motor learning ability. We also assessed the effects of WL and GA on the antioxidant profile, cytotoxicity, apoptosis, excitotoxicity, inflammatory cascades, and on growth factors which helps in neurogenesis. The compounds effectively improved the motor function, motor learning memory in the rats. Similarly, enhanced the activity of Glutathione peroxidase, SOD, catalase, and declined the lipid peroxidation and nitrite production in the brain. The treatment with WL and GA lowered the activities of LDH, m‐calpain, and caspase‐3. The reports strongly support that both compounds are useful in the prevention of glutamate excitotoxicity induced by QUIN. The NAA, IGF‐1, and VEGF levels in the brain were improved after treatment with WL and GA. The neuroprotective effects of WL and GA further proved through the anti‐inflammatory effects. The compounds significantly down‐regulated the expression of TNF‐&agr;, IL‐6, and IL‐&bgr; in the brain. Immunohistochemical analysis shows that the WL and GA reduced the expression of NF‐&kgr;B. The histopathological studies for cerebellum, hippocampus, striatum, and spinal cord confirms the toxic effects of QUIN and neuroprotective effects of WL and GA. The results suggest that WL and GA could ameliorate the toxic events triggered by QUIN and might be effective in the prevention and progression of several cascades which lead to the development of sALS.

Assessment of neuroprotective effects of Gallic acid against glutamate-induced neurotoxicity in primary rat cortex neuronal culture

ABSTRACT Glutamate excitotoxicity plays a crucial role in the pathogenesis behind the development and progression of several neurodegenerative diseases. The study aimed to investigate the neuroprotective activity of Gallic acid (GA) against glutamate‐induced neurotoxicity in primary rat cortex neurons (RCN). Treated the RCNs with GA 25 & 50 &mgr;g/ml for 2 h and later treated the cells with 100 &mgr;M glutamate (GLU) and incubated for 24 h at 37 °C. The results demonstrated that, the GA improved the antioxidant profile in the cortex neurons and inhibited the production of the proinflammatory cytokine. GA also maintained the Ca2+ homeostasis, IGF‐1 expression, and protected the neurons from glutamate‐induced neuronal toxicity. The neuroprotective activity of GA has further confirmed from the results of N‐acetylaspartate and expression of microtubule‐associated protein‐2 expression. The reports suggest that, GA is significantly attenuated the glutamate‐induced neurotoxicity and protected neurons from various chemical events that are involved in the pathogenesis of neurotoxicity. HighlightsGlutamate excitotoxicity is a major pathogenesis behind the development and progression of neurodegenerative diseases.Glutamate‐induced neurotoxicity in RCN is mediated through the formation of free radicles and proinflammatory cytokine.Glutamate treatment also caused an alteration in Ca2+ homeostasis and decline in IGF‐1 level.Observed a down‐regulation of MAP‐2 expression and NAA concentration in glutamate treated rat cortex neurons.Treatment with GA improved the antioxidant status in neurons and inhibited proinflammatory cytokine production.GA also maintained the Ca2+ homeostasis, IGF‐1 expression, and protected neurons from glutamate‐induced neuronal toxicity.

Comprehensive Assignments of Extraction, Isolation and Characterization of Taraxerol from Bark Annona reticulata L. and Chemopreventive Effect on Human Prostate Cancer Cell Lines (lncap and pc-3)

Prostate Cancer (PC) ruins a foremost cause of death of males in the US as well its growth rate is increased in the rest of the world. The current learning aims to perform a preliminary photochemical analysis by the successive extraction of the bark of Annona reticulata L. using petroleum ether, chloroform, and ethanol. The isolation, structure elucidation and identification of Taraxerol and check up in vitro study in prostate carcinoma. The structure was elucidated by spectroscopic techniques included Thin Layer chromatography (TLC) and High Performance Liquid Chromatography (HPLC), UV and Gas Chromatography-Mass Spectrometric (GC-MS). The prostate cell lines, LNCaP and PC-3 cell lines was cultured and antiproliferative effect by MTT Method, Neutral red cytotoxicity, measurement of LDH release, determinations of apoptosis by Acridine Orange (AO) and Ethidium Bromide (EB) double staining. Inhibition of protein denaturation, caspase levels by indirect ELISA and DNA fragmentation was performed. Investigation of the phytochemical summary on the bark of A. reticulata L. reports the occurrence of flavonoids, saponins, triterpenoid and tannins. In-vitro experiments show the selected compound exhibited of cytotoxicity against the cancer cell lines. An increase in caspase activity or caspase levels is generally considered as indicators of cellular apoptosis. The compounds to prevent heat associated denaturation of albumin are measured as a screening method for assessing anti-inflammatory potential of compounds.