Phytomedicinal Role of Pithecellobium dulce

Present study investigates the beneficial role of the aqueous extract of the fruits of Pithecellobium dulce (AEPD) against carbon tetrachloride (CCl4)-induced hepatic injury using a murine model. AEPD has been found to possess free radical (DPPH, hydroxyl and superoxide) scavenging activity in cell-free system. CCl4 exposure increased the activities of various serum maker enzymes and intracellular reactive oxygen species (ROS) production. In line with these findings, we also observed that CCl4 intoxication increased the lipid peroxidation and protein carbonylation accompanied by decreased intracellular antioxidant defense, activity of cytochrome P450 and CYP2E1 expression. DNA fragmentation and flow cytometric analyses revealed that CCl4 exposure caused hepatic cell death mainly via the necrotic pathway. Treatment with AEPD both pre- and post-toxin exposure protected the organ from CCl4-induced hepatic damage. Histological findings also support our results. A well-known antioxidant vitamin C was included in this study to compare the antioxidant potency of AEPD. Combining all, results suggest that AEPD protects murine liver against CCl4-induced oxidative impairments probably via its antioxidative property

ESTIMATION OF ALKALOIDS AND PHENOLICS OF FIVE EDIBLE CUCURBITACEOUS PLANTS AND THEIR ANTIBACTERIAL ACTIVITY

Objective: Objective of the present work was qualitative and quantitative estimation of alkaloids and phenolics of five edible cucurbitaceous plants and to evaluate their antibacterial activity against some human pathogenic bacteria.Methods: Total alkaloid present was determined by acid-based titrimetric methods using methyl red as an indicator and observing a faint yellow end point. Total phenolics were estimated by follin-ciocaltue's method using tannic acid as standard. Antibacterial activity was determined by Disc diffusion method using SRL Agar medium. The 70% ethanolic dried powdered was dissolved in 20% DMSO at different concentration to carry out the anti-microbial activity.Results: It was found that all the experimental plants contained almost equal amount of alkaloids but their phenolic contents as tannic acid equivalents were different. Alkaloids content of five Cucurbitaceous plants were found to vary from 1.15 g % to 1.34 g % and phenol content was varied from 4.54 mg/g to 10.13 mg/g. All the selected Cucurbitaceous plants were active against the tested pathogens, except against V. cholerae non.0139 (L4). Only the 70% ethanolic leaf extract of Momordica charantia (Linn.) showed a relative percentage inhibition from 15.02 to 16.63. So, Momordica charantia (Linn.) extract was the most active among five selected plants against the tested pathogens.Conclusion: The activity might be due to the presence of alkaloids and phenols. However, the extent of activity or zone of inhibition was found varied for different extracts might be due to the difference in the constituents present in the plant extracts

Amelioration of galactosamine-induced nephrotoxicity by a protein isolated from the leaves of the herb, Cajanus indicus L

<p>Abstract</p> <p>Background</p> <p>Galactosamine (GalN), an established experimental toxin, mainly causes liver injury via the generation of free radicals and depletion of UTP nucleotides. Renal failure is often associated with end stage liver damage. GalN intoxication also induces renal dysfunction in connection with hepatic disorders. Present study was designed to find out the effect of a protein isolated from the leaves of the herb <it>Cajanus indicus </it>against GalN induced renal damage.</p> <p>Methods</p> <p>Both preventive as well as curative effect of the protein was investigated in the study. GalN was administered intraperitoneally at a dose of 800 mg/kg body weight for 3 days pre and post to protein treatment at an intraperitoneal dose of 2 mg/kg body weight for 4 days. The activities of antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione-S-transferase (GST), levels of cellular metabolites, reduced glutathione (GSH), total thiols, oxidized glutathione (GSSG) and lipid peroxidation end products were determined to estimate the status of the antioxidative defense system. In addition, serum creatinine and urea nitrogen (UN) levels were also measured as a marker of nephrotoxicity.</p> <p>Results</p> <p>Results showed that GalN treatment significantly increased the serum creatinine and UN levels compared to the normal group of mice. The extent of lipid peroxidation and the level of GSSG were also enhanced by the GalN intoxication whereas the activities of antioxidant enzymes SOD, CAT, GR and GST as well as the levels of total thiols and GSH were decreased in the kidney tissue homogenates. Protein treatment both prior and post to the toxin administration successfully altered the effects in the experimental mice.</p> <p>Conclusion</p> <p>Our study revealed that GalN caused a severe oxidative insult in the kidney. Protein treatment both pre and post to the GalN intoxication could protect the kidney tissue against GalN induced oxidative stress. As GalN induced severe hepatotoxicity followed by renal failure, the protective role of the protein against GalN induced renal damages is likely to be an indirect effect. Since the protein possess hepatoprotective activity, it may first ameliorate GalN-induced liver damage and consequently the renal disorders are reduced. To the best of our knowledge, this is probably the first report describing GalN-induced oxidative stress in renal damages and the protective role of a plant protein molecule against it.</p

Protective Role of Taurine against Arsenic-Induced Mitochondria-Dependent Hepatic Apoptosis via the Inhibition of PKCδ-JNK Pathway

BACKGROUND: Oxidative stress-mediated hepatotoxic effect of arsenic (As) is mainly due to the depletion of glutathione (GSH) in liver. Taurine, on the other hand, enhances intracellular production of GSH. Little is known about the mechanism of the beneficial role of taurine in As-induced hepatic pathophysiology. Therefore, in the present study we investigated its beneficial role in As-induced hepatic cell death via mitochondria-mediated pathway. METHODOLOGY/PRINCIPAL FINDINGS: Rats were exposed to NaAsO(2) (2 mg/kg body weight for 6 months) and the hepatic tissue was used for oxidative stress measurements. In addition, the pathophysiologic effect of NaAsO(2) (10 microM) on hepatocytes was evaluated by determining cell viability, mitochondrial membrane potential and ROS generation. As caused mitochondrial injury by increased oxidative stress and reciprocal regulation of Bcl-2, Bcl-xL/Bad, Bax, Bim in association with increased level of Apaf-1, activation of caspase 9/3, cleavage of PARP protein and ultimately led to apoptotic cell death. In addition, As markedly increased JNK and p38 phosphorylation with minimal disturbance of ERK. Pre-exposure of hepatocytes to a JNK inhibitor SP600125 prevented As-induced caspase-3 activation, ROS production and loss in cell viability. Pre-exposure of hepatocytes to a p38 inhibitor SB2035, on the other hand, had practically no effect on these events. Besides, As activated PKCdelta and pre-treatment of hepatocytes with its inhibitor, rottlerin, suppressed the activation of JNK indicating that PKCdelta is involved in As-induced JNK activation and mitochondrial dependent apoptosis. Oral administration of taurine (50 mg/kg body weight for 2 weeks) both pre and post to NaAsO(2) exposure or incubation of the hepatocytes with taurine (25 mM) were found to be effective in counteracting As-induced oxidative stress and apoptosis. CONCLUSIONS/SIGNIFICANCE: Results indicate that taurine treatment improved As-induced hepatic damages by inhibiting PKCdelta-JNK signalling pathways. Therefore taurine supplementation could provide a new approach for the reduction of hepatic complication due to arsenic poisoning

Aqueous extract of Terminalia arjuna prevents carbon tetrachloride induced hepatic and renal disorders

BACKGROUND: Carbon tetrachloride (CCl(4)) is a well-known hepatotoxin and exposure to this chemical is known to induce oxidative stress and causes liver injury by the formation of free radicals. Acute and chronic renal damage are also very common pathophysiologic disturbances caused by CCl(4). The present study has been conducted to evaluate the protective role of the aqueous extract of the bark of Termnalia arjuna (TA), an important Indian medicinal plant widely used in the preparation of ayurvedic formulations, on CCl(4 )induced oxidative stress and resultant dysfunction in the livers and kidneys of mice. METHODS: Animals were pretreated with the aqueous extract of TA (50 mg/kg body weight) for one week and then challenged with CCl(4 )(1 ml/kg body weight) in liquid paraffin (1:1, v/v) for 2 days. Serum marker enzymes, namely, glutamate pyruvate transaminase (GPT) and alkaline phosphatase (ALP) were estimated in the sera of all study groups. Antioxidant status in both the liver and kidney tissues were estimated by determining the activities of the antioxidative enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST); as well as by determining the levels of thiobarbutaric acid reactive substances (TBARS) and reduced glutathione (GSH). In addition, free radical scavenging activity of the extract was determined from its DPPH radical quenching ability. RESULTS: Results showed that CCl(4 )caused a marked rise in serum levels of GPT and ALP. TBARS level was also increased significantly whereas GSH, SOD, CAT and GST levels were decreased in the liver and kidney tissue homogenates of CCl(4 )treated mice. Aqueous extract of TA successfully prevented the alterations of these effects in the experimental animals. Data also showed that the extract possessed strong free radical scavenging activity comparable to that of vitamin C. CONCLUSION: Our study demonstrated that the aqueous extract of the bark of TA could protect the liver and kidney tissues against CCl(4)-induced oxidative stress probably by increasing antioxidative defense activities

Synthesis of Ultra-small size Orthorhombic CsPbBr3 Perovskite Nanocrystal

Synthesis of ultra-small and colloidal stable CsPbBr3 NCs with high PLQY and significant lifetime is a challenge indeed. In this study we have synthesized CsPbBr3 materials (TBIA-CsPbBr3, DBIA-CsPbBr3, DBHT-CsPbBr3, and NBS-CsPbBr3) obtained via hot injection methods employing TBIA (tribromoisocyanuric acid), DBIA (dibromoisocyanuric acid), DBHT (1,3-dibromo-5,5-dimethylhydantoin), NBS (N-bromosuccinamide) as the external bromine precursors. The TBIA-CsPbBr3 is found to have the smallest dimension (ultra-small ~5.6 nm) among these four. The outstanding traits exhibited by these NCs highlight their immense potential for practical applications across diverse fields

An economic order quantity model with ramp type demand rate, constant deterioration rate and unit production cost

We have developed an order level inventory system for deteriorating items with demand rate as a ramp type function of time. The finite production rate is proportional to the demand rate and the deterioration rate is independent of time. The unit production cost is inversely proportional to the demand rate. The model with no shortages case is discussed considering that: (a) the demand rate is stabilized after the production stopping time and (b) the demand is stabilized before the production stopping time. Optimal costs are determined for two different cases