A review: Oligodendrocytes in neuronal axonal conduction and methods for enhancing their performance.

OBJECTIVES: This review explores the vital role of oligodendrocytes in axon myelination and efficient neuronal transmission and the impact of dysfunction resulting from neurotransmitter deficiencies related disorders. Furthermore, the review also provides insight into the potential of bionanotechnology for addressing neurodegenerative diseases by targeting oligodendrocytes. METHODS: A review of literature in the field was conducted using Google scholar. Systematic searches were performed to identify relevant studies and reviews addressing the role of oligodendrocytes in neural function, the influence of neurotransmitters on oligodendrocyte differentiation, and the potential of nanotechnology-based strategies for targeted therapy of oligodendrocytes. RESULTS: This review indicates the mechanisms underlying oligodendrocyte differentiation and the influence of neurotransmitters on this process. The importance of action potentials and neurotransmission in neural function and the susceptibility of damaged nerve axons to ischemic or toxic damage is provided in detail. The potential of bionanotechnology for targeting neurodegenerative diseases using nanotechnology-based strategies, including polymeric, lipid-based, inorganic, organic, and biomimetic nanoparticles, suggests better management of neurodegenerative disorders. CONCLUSION: While nanotechnology-based biomaterials show promise for targeted oligodendrocyte therapy in addressing neurodegenerative disorders linked to oligodendrocyte dysfunction, encapsulating neuroprotective agents within nanoparticles offers additional advantages. Nano-based delivery systems effectively protect drugs from degradation and prolong their therapeutic effects, holding promise in overcoming the blood-brain barrier by facilitating drug transport. However, a multifaceted approach is essential to enhance oligodendrocyte differentiation, promote myelin repair, and facilitate myelin dynamics with reduced toxicity. Further research is needed to elucidate the optimal therapeutic approaches and enhance patient outcomes.

Anti-Aging Strategies And Topical Delivery Of Biopolymer-Based Nanocarriers For Skin Cancer Treatment.

BACKGROUND: Environmental factors like UV radiation and epigenetic changes are one of the major factors for skin cancer that triggers aging. This review provides basic information on cancer development with respect to aging the receptors involved and the therapeutic targets. OBJECTIVE: Biopolymers like polysaccharide, polyphenols, proteins, nucleic acid plays a vital role in regulation of normal cell homeostasis. It is therefore pertinent to explore the role of biopolymers as antiaging formulations and also the possibility of these formulations used against cancer via topical administrations. METHODS: As UV radiation is one of the predominant factor in causing skin cancer the association of receptors between aging and cancer indicated that insulin receptor, melatonin receptor, toll like receptor, sirtuin 1 receptor, tumor specific T cell receptor and mitochondria based targeting can be used to direct therapeutics for suppression of cancer and prevent aging. RESULTS: Biopolymer based nanoformulations have tremendously progressed by entrapment of drugs like curcumin, resveratrol which can prevent cancer and aging in a similar mechanism. CONCLUSION: Certain protein signalling or calcium and ROS signalling pathways are different for cancer and aging process. The involvement of mitochondrial DNA mutation along with telomere shortening with a change in cellular energetics leading to genomic instability in aging process can also induce mitochondrial dysfunction and epigenetic alterations leading to skin cancer. Therefore, the use of biopolymers as a topical supplement during aging process can result in the prevention of cancer.

Targeting colon cancer stem cells using novel doublecortin like kinase 1 antibody functionalized folic acid conjugated hesperetin encapsulated chitosan nanoparticles.

The cancer stem cell (CSC) hypothesis is an evolving oncogenesis concept. CSCs have a distinct ability to self-renew themselves and also give rise to a phenotypically diverse population of cells. Targeting CSCs represents a promising strategy for cancer treatment. Plant-derived compounds are potent in restricting the expansion of CSCs. DCLK1 has been already reported as a colon CSC specific marker. Nanoparticles can effectively inhibit multiple types of CSCs by targeting specific markers. We have synthesized DCLK1 functionalized folic acid conjugated hesperetin encapsulated chitosan nanoparticles (CFH-DCLK1), specifically to target CSCs. In this regard, we have performed proliferation assay, colony formation assay, cell migration assay, apoptosis assay, flow cytometry analysis, real-time RT- PCR and western blot analyses to determine the effect of CFH-DCLK1 and CFH nanoparticles in HCT116-colon cancer cells. In our study, we have determined the median inhibitory concentration (IC50) of CFH (47.8 µM) and CFH-DCLK1 (4.8 µM) nanoparticles in colon cancer cells. CFH-DCLK1 nanoparticles induced apoptosis and inhibited the migration and invasion of colon cancer cells. Real time PCR and western blot results have demonstrated that the treatment with CFH-DCLK1 nanoparticles significantly reduced the expression of CSC markers such as DCLK1, STAT1 and NOTCH1 compared to the CFH alone in HCT116 colon cancer cells. Finally, in the 3D spheroid model, CFH-DCLK1 nanoparticles significantly inhibited the colonosphere growth. Overall, our results highlight the effectiveness of CFH-DCLK1 nanoparticles in targeting the colon cancer cells and CSCs. This study would lead to the development of therapies targeting both cancer cells and CSCs simultaneously using nanoformulated drugs, which could bring changes in the current cancer treatment strategies.

Potent antifungal agents and use of nanocarriers to improve delivery to the infected site: A systematic review.

There are four major classes of antifungals with the predominant mechanism of action being targeting of cell wall or cell membrane. As in other drugs, low solubility of these compounds has led to low bioavailability in target tissues. Enhanced drug dosages have effects such as toxicity, drug-drug interactions, and increased drug resistance by fungi. This article reviews the current state-of-the-art of antifungals, structure, mechanism of action, other usages, and toxic side effects. The emergence of nanoformulations to transport and uniformly release cargo at the target site is a boon in antifungal treatment. The article details research that lead to the development of nanoformulations of antifungals and potential advantages and avoidance of the lacunae characterizing conventional drugs. A range of nanoformulations based on liposomes, polymers are in various stages of research and their potential advantages have been brought out. It could be observed that under similar dosages, test models, and duration, nanoformulations provided enhanced activity, reduced toxicity, higher uptake and higher immunostimulatory effects. In most instances, the mechanism of antifungal activity of nanoformulations was similar to that of regular antifungal. There are possibilities of coupling multiple antifungals on the same nano-platform. Increased activity coupled with multiple mechanisms of action presents for nanoformulations a tremendous opportunity to overcome antifungal resistance. In the years to come, robust methods for the preparation of nanoformulations taking into account the repeatability and reproducibility in action, furthering the studies on nanoformulation toxicity and studies of human models are required before extensive use of nanoformulations as a prescribed drug.

5-Azacytidine incorporated polycaprolactone-gelatin nanoscaffold as a potential material for cardiomyocyte differentiation.

India has an alarming rate of growth of cardiovascular diseases (CVD). Similar to cancer there is a significant role for epigenetic factors in the increasing prevalence of CVD. Targeting the epigenetic mechanism, viz., the DNA methylation processes, histone modifications, and RNA based arrangements is today considered as a potential therapeutic approach to CVD management. 5-Azacytidine is an epigenetic treatment drug that is involved in the demethylation of DNA. 5-Azacytidine is an FDA approved drug for myelodysplastic syndrome. However, the usage of 5-Azacytidine for CVD has not been found acceptable because of its poor stability in neutral solutions and shorter half-live which makes it toxic to the cells. A significant breakthrough in the use of 5-azacytidine for cell therapy and tissue engineering for CVD treatment has been gained based on its ability to differentiate mesenchymal stem cells into cardiomyocytes. This work addresses the further need for a sustained release of this drug, to reduce its toxicity to the stem cells. Electrospun PCL-gelatin fibres that are well aligned to provide a mat-like structure with sufficient porosity for differentiated cells to move forward have been synthesized. The crystalline character, porosity, fibre width, thermal behavior hydrophilicity of these scaffolds are in tune with those reported in the literature as ideal for cell proliferation and adhesion. FTIR measurements confirm the entrapment of 5-azacytidine on to the scaffold. The adsorption of the drug did not alter the characteristic features of the scaffold. Primary results on cell viability and cell morphology, as well as cardiomyocyte differentiation, have shown that PCL-gelatin scaffolds carrying 5-azacytidine developed in this work could serve as an ideal platform for mesenchymal stem cell differentiation into cardiomyocytes.

Chlorogenic acid- loaded calcium phosphate chitosan nanogel as biofilm degradative materials.

This work describes an effort to develop an antimicrobial agent (chlorogenic acid - CGA) loaded porous nanogel based on calcium phosphate-chitosan (CaPNP@Chi) nanogel with biofilm degradative properties and has potential applications in restorative dentistry. The nanogel was prepared by ionic gelation of calcium phosphate nanoparticles and chitosan in the ratio of 1.25: 1. Chlorogenic acid was loaded to the nanoparticles as an ethanolic solution and the encapsulation efficiency determined by chromatographic techniques. The particle size and morphology of CaPNP@Chi and CaPNP@Chi@CGA was determined by dynamic light scattering and scanning electron microscopic techniques. The minimum inhibitory concentration against S. aureus and K. pneumoniae was determined through the well diffusion method. The biofilm formation and biofilm decay were studied through staining assays. The toxicity, if any of the nanogel was assessed by MTT assay against HaCaT cells. All data were statistically analyzed. The composite had a CGA encapsulation efficiency of 70% and was thermally stable up to 124 °C. The zone of inhibition was found to be 18.7 mm ± 0.6 against S. aureus. CaPNP@Chi@CGA showed a 68% increase in biofilm degradation when compared with the untreated group. Results obtained in this study suggest that the positively charged nanogel interacted with the bacterial cell membrane and brought about the disruption of the cell membrane. Also, CaPNP@Chi@CGA was observed to be nontoxic up to 40 µg/mL to HaCaT cells. These results support the potential of CaPNP@Chi@CGA nanogel for biofilm degradation and its application as filling material in restorative dentistry.

Lithium entrapped chitosan nanoparticles to reduce toxicity and increase cellular uptake of lithium.

Lithium carbonate is an effective drug against bipolar disorders. Direct use of lithium carbonate has been reported to result in lithium toxication and pulmonary complications. With chitosan micro and nanoparticles gaining attention for their protein absorption, drug targeting and improved dissolution rate of sparingly water-soluble drugs, this work has focused on chitosan loaded Li as a possible alternative to Li alone for cellular uptake. Well standardized ionic gelation technique employed in this study resulted in Li loaded chitosan nanoparticles with hydrodynamic diameter below 300 nm and zeta potential of + 30 mV and oval morphology. Through various techniques electrostatic interaction as well as Claritin dependent endocytic pathway is suggested as facilitating 1.3 times increase in cell proliferation in lithium carbonate loaded chitosan nanoparticles treated PC12 cells. A controlled Li release to the extent of less than 50% in 48 h from the nanoparticle was observed. This observation has very high significance as it ensures that the lithium toxicity can be avoided. These results indicated that chitosan is a promising carrier for lithium carbonate and may improve its therapeutic efficacy and also overcome toxicity during its use in the treatment of neuropsychiatric disorders.

Chitosan-based nano-formulation enhances the anticancer efficacy of hesperetin.

Cancer is one of the major causes of increased morbidity and mortality in modern society. Colorectal cancer is the third leading cause for cancer related death worldwide. Current chemotherapeutics are not very effective and have severe side effects. Hesperetin is a bioflavonoid from citrus fruits and its clinical use is restricted because of the poor water solubility. Folate receptor is overexpressed in various cancer cells. Therefore, we synthesized the chitosan folate hesperetin nanoparticle (CFH) by covalently conjugating folic acid with chitosan molecules. The size of the CFH nanoparticles is around 450nm, which is advantageous for passively targeting the cancer cell specifically due to the leaky vasculature of the tumour. Particle surface and size were observed using SEM and TEM studies. The results show that hesperetin has an IC50 value of 190µM and it induces apoptosis in HCT15 cells, however, CFH is very potent in inhibiting the proliferation with the IC50 value of 28µM. In addition, CFH inhibited colony formation and induced apoptosis by regulating the expression of proapoptotic genes expression. Therefore, the chitosan - folic acid conjugation appears to be the suitable carrier for colorectal cancer cell-specific delivery of hesperetin.

Role of nanoparticle size in self-assemble processes of collagen for tissue engineering application.

Nanoparticle mediated extracellular matrix may offer new and improved biomaterial to wound healing and tissue engineering applications. However, influence of nanoparticle size in extracellular matrix is still unclear. In this work, we synthesized different size of silver nanoparticles (AgNPs) comprising of 10nm, 35nm and 55nm using nutraceuticals (pectin) as reducing as well as stabilization agents through microwave irradiation method. Synthesized Ag-pectin nanoparticles were assimilated in the self-assemble process of collagen leading to fabricated collagen-Ag-pectin nanoparticle based scaffolds. Physico-chemical properties and biocompatibility of scaffolds were analyzed through FT-IR, SEM, DSC, mechanical strength analyzer, antibacterial activity and MTT assay. Our results suggested that 10nm sized Ag-pectin nanoparticles significantly increased the denaturation temperature (57.83°C) and mechanical strength (0.045MPa) in comparison with native collagen (50.29°C and 0.011MPa). The in vitro biocompatibility assay reveals that, collagen-Ag-pectin nanoparticle based scaffold provided higher antibacterial activity against to Gram positive and Gram negative as well as enhanced cell viability toward keratinocytes. This work opens up a possibility of employing the pectin caged silver nanoparticles to develop collagen-based nanoconstructs for biomedical applications.

Direct observation of redox reactions in Candida parapsilosis ATCC 7330 by Confocal microscopic studies.

Confocal microscopic studies with the resting cells of yeast, Candida parapsilosis ATCC 7330, a reportedly versatile biocatalyst for redox enzyme mediated preparation of optically pure secondary alcohols in high optical purities [enantiomeric excess (ee) up to >99%] and yields, revealed that the yeast cells had large vacuoles under the experimental conditions studied where the redox reaction takes place. A novel fluorescence method was developed using 1-(6-methoxynaphthalen-2-yl)ethanol to track the site of biotransformation within the cells. This alcohol, itself non-fluorescent, gets oxidized to produce a fluorescent ketone, 1-(6-methoxynaphthalen-2-yl)ethanone. Kinetic studies showed that the reaction occurs spontaneously and the products get released out of the cells in less time [5 mins]. The biotransformation was validated using HPLC.

Whole resting cells vs. cell free extracts of Candida parapsilosis ATCC 7330 for the synthesis of gold nanoparticles.

The cell free extracts of Candida parapsilosis ATCC 7330 are more efficient than the whole resting cells of the yeast in the synthesis of directly usable gold nanoparticles as revealed by this systematic study. Cell free extracts yielded gold nanoparticles of hydrodynamic diameter (50-200 nm). In this study, the total protein concentration influences the nanofabrication and not only the reductase enzymes as originally thought. Powder X-ray diffraction studies confirm the crystalline nature of the gold nanoparticles. Fourier Transform Infra Red spectroscopy and thermal gravimetric analysis suggests that the biosynthesized gold nanoparticles are capped by peptides/proteins. Dispersion experiments indicate a stable dispersion of gold nanoparticles in pH 12 solutions which is also confirmed by electron microscopic analysis and validated using a surface plasmon resonance assay. The effectiveness of the dispersed nanoparticles for the reduction of 4-nitrophenol using sodium borohydride as a reductant further confirms the formation of functional gold nanoparticles. It is also reported that gold nanoparticles with mean particle diameter of 27 nm are biosynthesized inside the whole cell by transmission electron microscopy analysis. With optimized reaction conditions, maximum gold bioaccumulation with the 24 h culture age of the yeast with cellular uptake of ~1010 gold atoms at the single cell level is achieved but it is not easy to extract the gold nanoparticles from the whole resting cells.

Acute rejection associated with donor-specific anti-MICA antibody in a highly sensitized pediatric renal transplant recipient.

Allograft rejection in HLA identical transplant recipients and in patients without detectable donor-specific anti-HLA antibodies has lead to the identification of non-HLA antigens as targets of the alloimmune response. MICA antigen has been recognized as an important non-HLA target in renal transplantation. Recent studies have shown that anti-MICA antibodies are associated with acute renal allograft rejection and failure. Current cross match procedures using donor lymphocytes fail to detect MICA antibodies. Transplant candidates are not routinely tested for pre-sensitization to MICA antigens nor are transplant donors typed for MICA alleles. Optimal classification and treatment of acute rejection associated with MICA antibody remains unknown. In this case report, we are the first to describe the clinical course and treatment of donor-specific MICA antibody associated with both Banff type II A ACR and AMR in a highly sensitized pediatric renal re-transplant recipient. This case also emphasizes the importance of pre-transplant screening for donor-specific MICA antibody especially in highly sensitized renal transplant patients.

Architectonics of phage-liposome nanowebs as optimized photosensitizer vehicles for photodynamic cancer therapy.

Filamentous M13 phage can be engineered to display cancer cell-targeting or tumor-homing peptides through phage display. It would be highly desirable if the tumor-targeting phage can also carry anticancer drugs to deliver them to the cancer cells. We studied the evolution of structures of the complexes between anionic filamentous M13 phage and cationic serum-stable liposomes that encapsulate the monomeric photosensitizer zinc naphthalocyanine. At specific phage-liposome ratios, multiple phage nanofibers and liposomes are interwoven into a "nanoweb." The chemical and biological properties of the phage-liposome nanoweb were evaluated for possible application in drug delivery. This study highlights the ability of phage-liposome nanowebs to serve as efficient carriers in the transport of photosensitizers to cancer cells.

Mechanism of protective action of mangiferin on suppression of inflammatory response and lysosomal instability in rat model of myocardial infarction.

Lysosomal instability has been suggested as a major factor in the development of cellular injury during myocardial necrosis through the formation of inflammatory mediators. The present study was designed to investigate the effect of mangiferin on lysosomal hydrolases and TNF-alpha production during isoproterenol (ISPH) induced myocardial necrosis in rats. The rats given ISPH (200 mg/kg body weight twice, subcutaneous) for 2 days showed a significant increase in plasma TNF-alpha production, serum and heart lysosomal hydrolases activity. ISPH administration to rats resulted in decreased stability of the membranes, which was reflected by the lowered activity of cathepsin-D and beta-glucuronidase in mitochondrial, nuclear, lysosomal and microsomal fractions. Pretreatment with mangiferin (100 mg/kg body weight, intraperitoneally) for 28 days, significantly prevented the alterations and restored the enzyme activities to near-normal status. These findings demonstrate that mangiferin could preserve lysosomal integrity through decrease in the inflammatory process and hence establish the cardioprotective effect of mangiferin.

Chemopreventive and therapeutic modulation of green tea polyphenols on drug metabolizing enzymes in 4-Nitroquinoline 1-oxide induced oral cancer.

Oral cancer is one of the most common cancers in the world. Drugs can modulate the expression of drug metabolizing enzymes and are useful in chemoprevention as well as therapy in cancer. 4-Nitroquinoline 1-oxide (4-NQO) is used to induce oral cancer in the present study. In the present investigation, the effect of green tea polyphenols (GTP) on the activities of cytochrome b5, cytochrome P450, cytochrome b5 reductase (cyt b5 R), cytochrome P450 reductase (cyt P450 R), arryl hydrocarbon hydroxylase (AHH), DT-diaphorase (DTD)(Phase I enzymes) and glutathione-S-transferase (GST) and UDP-glucuronyl transferase (UDP-GT) (Phase II enzymes) were assessed in tongue and oral cavity. In induced rats, there was a decrease in the activity of Phase II enzymes and an increase in the activity of Phase I enzymes. On supplementation of GTP by both simultaneous and post treatment mode (200mg/kg) there was a significant increase in the activity of GST and UDP-GT and a significant decrease in the activity of Phase I enzymes. There was a significant decline in the number of tumors, tumor volume and oral squamous cell carcinoma in both simultaneous and post GTP treated animals relative to 4-NQO induced animals; on comparing simultaneous and post GTP treated animals the number of tumors, tumor volume and oral squamous cell carcinoma was significantly reduced in post treated animals. Thus inhibition of Phase I enzymes could be attributed to the protective efficacy of GTP which deactivates carcinogen and GTP induced the expression of Phase II enzymes that detoxifies the 4-NQO. It can be proposed that GTP plays role as a detoxifying agent by which its modulating role prevented/inhibited the formation of tumor.

Role of Pterocarpus santalinus against mitochondrial dysfunction and membrane lipid changes induced by ulcerogens in rat gastric mucosa.

Free radicals produced by ulcerogenic agents affect the TCA cycle enzymes located in the outer membrane of the mitochondria. Upon induction with ulcerogens, peroxidation of membrane lipids bring about alterations in the mitochondrial enzyme activity. This indicates an increase in the permeability levels of the mitochondrial membrane. The ability of PSE to scavenge the reactive oxygen species results in restoration of activities of TCA cycle enzymes. NSAIDs interfere with the mitochondrial beta-oxidation of fatty acids in vitro and in vivo, resulting in uncoupling of mitochondrial oxidative phosphorylation process. This usually results in diminished cellular ATP production. The recovery of gastric mucosal barrier function through maintenance of energy metabolism results in maintenance of ATP levels, as observed in this study upon treatment with PSE. Membrane integrity altered by peroxidation is known to have a modified fatty acid composition, a disruption of permeability, a decrease in electrical resistance, and increase in flip-flopping between monolayers and inactivated cross-linked proteins. The severe depletion of arachidonic acid in ulcer induced groups was prevented upon treatment with PSE. The acid inhibitory property of the herbal extract enables the maintenance of GL activity upon treatment with PSE. The ability to prevent membrane peroxidation has been traced to the presence of active constituents in the PSE. In essence, PSE has been found to prevent mitochondrial dysfunction, provide mitochondrial cell integrity, through the maintenance of lipid bilayer by its ability to provide a hydrophobic character to the gastric mucosa, further indicating its ability to reverse the action of NSAIDs and mast cell degranulators in gastric mucosa.

Ulcer protective effect of Terminalia arjuna on gastric mucosal defensive mechanism in experimental rats.

The methanol extract of the bark of Terminalia arjuna (Combretaceae) (TAE) showed marked antiulcer and ulcer healing activity against 80% ethanol (ETH), diclofenac sodium (DIC) and dexamethasone (DEX) induced ulcer models dose dependently at doses of 100, 400 and 200 mg/kg body weight respectively. Pre-, post and co-administration of TAE offered 100% protection to the gastric mucosa against ETH, DIC and DEX induced ulcers as observed from the ulcer score. Gastric mucosal analysis of DEX induced rats were associated with changes in the levels of protein, protein bound carbohydrate complexes, lipid peroxides (LPO), glutathione (GSH) and activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) compared with control rats. Co-administration with TAE in DEX rats (DEX + TAE) favorably altered the levels of LPO, GSH and also the activities of SOD and CAT in gastric mucosa, whereas the activities of GPx remained unaltered in all groups. In DEX + TAE rats, the levels of protein and protein bound carbohydrate complexes were increased when compared with DEX rats. The results indicate that the gastroprotective effect of TAE is probably related to its ability to maintain the membrane integrity by its antilipid peroxidative activity that protects the gastric mucosa against oxidative damage and its ability to strengthen the mucosal barrier, the first line of defense against exogenous and endogenous ulcerogenic agents.

Gastroprotective effect of Terminalia arjuna bark on diclofenac sodium induced gastric ulcer.

AIM: The present study was aimed to evaluate the effect of methanolic extract of Terminalia arjuna (TA) on diclofenac sodium induced gastric ulcer in experimental rats. METHODS: Animals were induced for gastric ulcer with diclofenac sodium (DIC) (80mg/kg bodyweight in water, orally) and treated orally with TA in various doses ranging from 100mg/kg bodyweight to 500mg/kg bodyweight. The effective dose was 400mg/kg bodyweight, since this dose elicited a maximum reduction in lesion index. The gastroprotective effect of TA was assessed from volume of gastric juice, pH, free and total acidity, pepsin concentration, acid output in gastric juice, the levels of non-protein sulfhydryls (NP-SH), lipid peroxide (LPO), reduced glutathione (GSH), and activities of enzymic antioxidants--super oxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and myeloperoxidase (MPO) in gastric mucosa. The levels of DNA, protein bound carbohydrate complexes--hexose, hexoseamine, sialic acid, fucose in gastric mucosa and gastric juice and the levels of RNA in gastric mucosa were assessed. The stomach tissues were used for adherent mucus content and also for the histological examination. RESULTS: A significant reduction in lesion index was observed in ulcer induced animals treated with TA (DIC+TA) compared to ulcerated rats (DIC). A significant increase was observed in pH, NP-SH, GSH, enzymic antioxidants, protein bound carbohydrate complexes, adherent mucus content, nucleic acids with a significant decrease in volume of gastric juice, free and total acidity, pepsin concentration, acid output, LPO levels and MPO activities in DIC+TA rats compared to DIC rats. Histological studies confirmed the gastroprotective activity of TA. CONCLUSION: From the data presented in this study it could be concluded that T. arjuna acts as an gastroprotective agent probably due to its free radical scavenging activity and cytoprotective nature.