Browsing by Author "D. Dash"

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Aldose reductase and diabetic retinopathy.
(1992) R. Singh; D. Dash; F.J. Ansari; O.P. Maurya; V.P. Singh
Serum aldose reductase activity was estimated spectrophotometrically in 25 normal subjects (Group A), 25 diabetic patients without retinopathy (Group B), and 25 diabetic patients with retinopathy (Group C). Serum aldose reductase levels were higher in diabetic patients with or without retinopathy than in normal subjects. Comparing the serum aldose reductase activity in diabetic patients with and without retinopathy showed the value was higher in the former group; this difference was statistically significant (P < .01). However, aldose reductase activity in proliferative and background retinopathy were equal and therefore not significant.
An antioxidant ameliorates allergic airway inflammation by inhibiting HDAC 1 via HIF-1α/VEGF axis suppression in mice
(Nature Research, 2023) Ramiya Islam; D. Dash; Rashmi Singh
Histone deacetylase inhibitors (HDACi) are novel class of drugs as they are involved in post translational modification of several proteins involved in signaling pathways related to asthma. HDACi have been reported to elicit protective effects on asthma but the signaling pathways associated with it have not been investigated much. Recently, we have demonstrated that intranasal administrations of Pan-HDAC inhibitors, sodium butyrate and curcumin, which have effectively reduced asthma severity via HDAC1 inhibition in Ovalbumin induced mouse model. Present study aimed to investigate possible pathways by which curcumin and sodium butyrate may minimize asthma pathogenesis via HDAC 1 inhibition. Balb/c mice were exposed (sensitized and challenged) with Ovalbumin to establish allergic asthma model followed by pretreatment of curcumin (5 mg/kg) and sodium butyrate (50 mg/kg) through intranasal route. Effects of curcumin and sodium butyrate on HIF-1α/VEGF signaling through activation of PI3K/Akt axis has been investigated using protein expressions followed by chromatin immunoprecipitation of BCL2 and CCL2 against HDAC1. Molecular docking analysis was also performed to investigate effects of curcumin and butyrate on mucus hypersecretion, goblet cell hyperplasia and airway hyperresponsiveness. Augmented expressions of HDAC-1, HIF-1α, VEGF, p-Akt and p-PI3K were observed in asthmatic group which was suppressed in both the treatments. NRF-2 level was significantly restored by curcumin and butyrate treatments. Protein expressions of p-p38, IL-5 and mRNA expressions of GATA-3 were also reduced in curcumin and butyrate treatment groups. Our findings suggest that curcumin and sodium butyrate may attenuate airway inflammation via down regulation of p-Akt/p-PI3K/HIF-1α/VEGF axis. © 2023, The Author(s).
Author Correction: An antioxidant ameliorates allergic airway inflammation by inhibiting HDAC 1 via HIF-1α/VEGF axis suppression in mice (Scientific Reports, (2023), 13, 1, (9637), 10.1038/s41598-023-36678-0)
(Nature Research, 2023) Ramiya Islam; D. Dash; Rashmi Singh
In the original version of this Article Rashmi Singh was incorrectly affiliated with ‘Department of Biochemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, India’. The correct affiliation is listed below. Department of Zoology, MMV, Banaras Hindu University, Varanasi 221005, India. The original Article has been corrected. © 2023, The Author(s).
Cilostazol reduces inflammatory burden and oxidative stress in hypertensive type 2 diabetes mellitus patients
(2007) Neeraj K. Agrawal; Rituparna Maiti; D. Dash; B.L. Pandey
Objectives: Inflammation and oxidative stress cause genesis and progression of atherosclerosis in diabetes. This study aimed to assess effects of Cilostazol on these factors in hypertensive type 2 diabetic patients. Materials and methods: In randomized, open, add-on preventive controlled clinical trial design, 60 hypertensive type 2 diabetics aged ≥45 years were evaluated clinically and for total leukocyte count, erythrocyte sedimentation rate, serum albumin, serum hsC-reactive protein, plasma malondialdehyde, blood reduced glutathione and HbA1c levels. After informed consent, 30 patients received Cilostazol (100 mg) twice daily orally as add-on therapy. At 1 month follow-up, 26 patients in control group and 22 patients in Cilostazol group completed the trial and particular parameters were re-evaluated. Results: The mean age and duration of diabetes were 55 ± 7 years and 8 ± 6 years, respectively. At follow-up, the Cilostazol group showed significant (p < 0.001) decrease in hsC-reactive protein (23.6%), erythrocyte sedimentation rate (38.7%), total leukocyte count (12.6%), plasma malondialdehyde (17.6%), HbA1c (0.17%, p = 0.002) and increase in serum albumin (11.9%), blood reduced glutathione (3.5%) from baseline. UKPDS 10 years risk of coronary heart disease decreased by 6% (p = 0.002). The control group did not show significant improvement in inflammatory profile, oxidative status and HbA1c. Conclusion: Inflammatory and oxidative stress is high in hypertensive type 2 diabetic patients. Cilostazol reduces these factors as well as coronary heart disease risk in diabetes mellitus. © 2007 Elsevier Ltd. All rights reserved.
Curcumin inhibits lipopolysaccharide (LPS)-induced endotoxemia and airway inflammation through modulation of sequential release of inflammatory mediators (TNF-α and TGF-β1) in murine model
(Birkhauser Verlag AG, 2017) Asha Kumari; D. Dash; Rashmi Singh
Objective: Curcumin (diferuloylmethane), a major component of turmeric is well known for its anti-inflammatory potential. Present study investigates sequential release of inflammatory mediators post LPS challenge (10 mg/kg,i.p.) causing lung inflammation and its modulation by curcumin through different routes (20 mg/kg, i.p and 10 mg/kg, i.n.) in murine model. Dexamethasone (1 mg/kg, i.p) was used as standard drug. Methods: Lung Inflammation was evaluated by histopathological analysis, myeloperoxidase (MPO) activity followed by inflammatory cell count and total protein content measurements in bronchoalveolar fluid (BALF). Reactive oxygen species (ROS), nitrite and TNF-α levels were measured as markers of endotoxin shock at different time points (1–72 h). The mRNA expression of transforming growth factors-β1 (TGF-β1), iNOS and Toll-like receptor-4 (TLR-4) were measured followed by Masson’s trichrome staining and hydroxyproline levels as collagen deposition marker leading to fibrotic changes in lungs. Results: We found that LPS-induced lung inflammation and injury was maximum 24-h post LPS challenge shown by MPO and histological analysis which was further supported by elevated nitrite and ROS levels whereas TNF-α level was highest after 1 h. Endotoxin-induced mortality was significantly reduced in curcumin (i.p) pretreatment groups up to 72-h post LPS challenge. Significant inhibition in mRNA expression of iNOS, TGF-β1 and TNF-α level was noted after curcumin treatment along with lowered MPO activity, inflammatory cell count, ROS, nitrite levels and collagen deposition in lungs. Conclusion: Our results suggest that higher endotoxin dose causes inflammatory mediator release in chronological order which tend to increase with time and reached maximum after 24-h post-endotoxin (LPS) exposure. Intraperitoneal route of curcumin administration was better in modulating inflammatory mediator release in early phase as compared to intranasal route of administration. It can be used as supplementary therapeutic intervention at early stage of endotoxemia, having fewer side effects. © 2017, Springer International Publishing.
Curcumin inhibits paraquat induced lung inflammation and fibrosis by extracellular matrix modifications in mouse model
(Birkhauser Verlag AG, 2016) Namitosh Tyagi; D. Dash; Rashmi Singh
Objective: Paraquat (PQ), a potent herbicide can cause severe toxicity. We report here that fibroproliferation phase of acute lung injury (ALI) is initiated much earlier (within 48 h) after PQ intoxication than previously reported (after 2 weeks) and we aimed to study the protective effects of intranasal curcumin as new therapeutic strategy in mouse model. Methods: Mice (Park's strain) were divided into five experimental groups (I) control, received only saline (0.9 % NaCl) (II) PQ, mice intoxicated with PQ (50 mg/kg, i.p., single dose); (III) curcumin, treated with curcumin (5 mg/kg, i.n) an hour before PQ administration; (IV)Veh, DMSO (equal volume to curcumin) given an hour before PQ exposure; (V) DEXA, mice treated with dexamethasone (1 mg/kg, i.p) before an hour of PQ intoxication. After 48 h of the PQ exposure, all mice were sacrificed and samples were analyzed. Results: Pretreatment with intranasal curcumin (5 mg/kg) could modify the PQ-intoxication (50 mg/kg, i.p) induced structural remodeling of lung parenchyma at an early phase of acute lung injury. Significant increase in inflammatory cell count, reactive oxygen species and hydroxyproline levels were decreased after curcumin pretreatment (all p < 0.05). Histological examination and zymography results were also found consistent. Conclusion: Our results show that curcumin pretreatment decreased the expression of alpha smooth muscle actin (α-SMA), matrix metalloproteinases-9 (MMP-9) and changed the expression of tissue inhibitors of metalloproteinase (TIMP-1) after PQ intoxication. Single toxic dose of PQ has initiated fibroproliferation within 48 h and intranasal curcumin may prove as new therapeutic strategy for PQ induced ALI and fibroproliferation. © 2016, Springer International Publishing.
Curcumin Modulates Paraquat-Induced Epithelial to Mesenchymal Transition by Regulating Transforming Growth Factor-β (TGF-β) in A549 Cells
(Springer New York LLC, 2019) Namitosh Tyagi; D.K. Singh; D. Dash; Rashmi Singh
Paraquat (PQ), a widely used potent herbicide, generates superoxide anions and other free radicals, leading to severe toxicity and acute lung injury. PQ induces pulmonary fibrosis through epithelial to mesenchymal transition (EMT) characterized by increased number of myofibroblasts. Time-dependent PQ-induced EMT has been evaluated in present investigation where intracellular ROS levels were significantly enhanced after 24 h of PQ intoxication. Anti-inflammatory effects of curcumin have been studied where alveolar epithelial cells (A549 cells) were incubated with curcumin (30 μΜ) for 1 and 3 h before PQ intoxication (700 μM). Western blot and immunocytochemistry studies revealed that pretreatment of A549 cells with curcumin for 3 h before PQ exposure has maintained E-cadherin expression and inhibited PQ induced α-smooth-muscle actin (α-SMA) expression. Transforming growth factor-β (TGF-β) that seems to be involved in PQ-induced EMT was enhanced after PQ intoxication, but curcumin pretreatment has effectively inhibited its expression. Immunostaining studies have shown that curcumin pretreatment has significantly reduced matrix metalloproteinase-9 (MMP-9) expressions, which were elevated after PQ intoxication. These results demonstrate that curcumin can regulate PQ-induced EMT by regulating the expression of TGF-β. © 2019, Springer Science+Business Media, LLC, part of Springer Nature.
Cytochrome P450 2E1 dependent catalytic activity and lipid peroxidation in rat blood lymphocytes
(2002) A. Dey; D. Parmar; A. Dhawan; D. Dash; P.K. Seth
To investigate the similarities in the catalytic activity of blood lymphocyte P450 2E1 in blood lymphocyte with the liver isoenzyme, NADPH dependent lipid peroxidation and activity of N-nitrosodimethyamine demethylase (NDMA-d) was studied in rat blood lymphocytes. Blood lymphocytes were found to catalyse NADPH dependent (basal) lipid peroxidation and demethylation of N-nitrosodimethylamine (NDMA). Pretreatment with ethanol or pyrazole or acetone resulted in significant increase in the NADPH dependent lipid peroxidation and the activity of NDMA-d in blood lymphocytes and liver microsomes. In vitro addition of CCl4 to the blood lymphocytes isolated from control or ethanol pretreated rats resulted in an increase in the NADPH dependent lipid peroxidation. Significant inhibition of the basal and CCl4 supported NADPH dependent lipid peroxidation and NDMA-d activity in blood lymphocytes isolated from control or ethanol pretreated rats by dimethyl formamide or dimethyl sulfoxide or hexane, solvents known to inhibit P450 2E1 catalysed reactions in liver and anti- P450 2E1, have indicated the role of P450 2E1 in the NADPH dependent lipid peroxidation in rat blood lymphocytes. The data indicating similarities in the NADPH dependent lipid peroxidation and NDMA-d activity in blood lymphocyte with the liver microsome have provided evidence that blood lymphocyte P450 2E1 could be used as a surrogate to monitor and predict hepatic levels of the enzyme. © 2002 Published by Elsevier Science Inc.
Differences in physical and biological properties of 50S ribosomes and 23S RNAs derived from tight and loose couple 70S ribosomes
(1984) D.P. Burma; A.K. Srivastava; S. Srivastava; D.S. Tewari; D. Dash; S.K. Sengupta
Tight couple (TC) 50S ribosomes on treatment with kethoxal lose their capacity to associate with 30S ribosomes whereas loose couple (LC) 50S ribosomes on such treatment fully retain their association capacity. The same is true for 23S RNAs isolated from treated 50S ribosomes or isolated 23S RNAs directly treated with kethoxal, so far as their capacity to associate with 16S RNA is concerned. At certain Mg++ concentrations TC 23S RNA is highly susceptible to the nucleolytic action of single-strand specific enzyme RNase I; LC 23S RNA is quite resistant. The Mg++-dependencies of the two species of 23S RNAs for association with 16S RNA are also quite different. The fluorescence enhancement of ethidium bromide due to binding to TC 23S RNA is slightly less than LC 23S RNA. The hyperchromicity of LC 23S RNA due to thermal denaturation is somewhat more than TC 23S RNA. LC 23S RNA has slightly more elliptic CD spectrum than TC 23S RNA. These results clearly show that 23S RNAs present in TC and LC 50S ribosomes are distinct from each other. It has been recently demonstrated in this laboratory that they can be interconverted by the agents involved in translocation and thus appear to be conformomers. © 1984.
Distribution and ethnic variation of â-thalassemia mutations in Nepal.
(2012) A. Mishra; A. Mukherjee; A. Roy; G. Singh; P. Shrestha; R.R. Singh; V. Rohil; N. Baral; S. Majhi; D. Dash
This is the first study characterizing spectrum of beta-thalassemia mutations in Nepalese population. Mutations were analyzed in 22 patients using 10 sets of allele-specific primers. Five of the mutations, namely F.S 41/42 (--TCTT), IVS1 nt5 (G-->C), IVS1 nt1 (G-->T), 619 bp deletion and F.S 8/9 (+G), were found to constitute 87.82% of total alleles studied. F.S 41/42 (--TCTT) was the commonest mutation. -88 (C-->T), Codon 16 (--C) and Codon 15 (G-->A), had a combined frequency of 12.18%. Distribution of mutations causing beta-thalassemia in different ethnic Nepalese groups was analyzed. The mutational profile in Nepal share several similarities with that from the two neighboring countries, India and China. Detection of more than one mutation in three cases of thalassemia trait raises the likelihood of existence of multiple mutations in cis in Nepalese thalassemic carriers. Such possibility has to be carefully considered while developing prenatal screening program for Nepalese population.
Do ribosomal RNAs act merely as scaffold for ribosomal proteins?
(Springer India, 1985) D.P. Burma; A.K. Srivastava; S. Srivastava; D. Dash; D.S. Tewari; B. Nag
Investigations that are being carried out in various laboratories including ours clearly provide the answer which is in the negative. Only the direct evidences obtained in this laboratory will be presented and discussed. It has been unequivocally shown that the interaction between 16S and 23S RNAs plays the primary role in the association of ribosomal subunits. Further, 23S RNA is responsible for the Binding of 5S RNA to 16S.23S RNA complex with the help of three ribosomal proteins, L5, L18, L15/L25. The 16S.23S RNA complex is also capable of carrying out the following ribosomal functions, although to small but significant extents, with the help of a very limited number of ribosomal proteins and the factors involved in protein synthesis: (a) poly U-Binding, (B) poly U-dependent Binding of phenylalanyl tRNA, (c) EF-G-dependent GTPase activity, (d) initiation complex formation, (e) peptidyl transferase activity (puromycin reaction) and (f) polyphenylalanine synthesis. These results clearly indicate the direct involvement of rRNAs in the various steps of protein synthesis. Very recently it has Been demonstrated that the conformational change of 23S RNA is responsible for the translocation of peptidyl tRNA from the aminoacyl (A) site to the peptidyl (P) site. A model has Been proposed for translocation on the Basis of direct experimental evidences. The new concept that ribosomal RNAs are the functional components in ribosomes and proteins act as control switches may eventually turn out to Be noncontroversial. © 1985 Printed in India.
Effect of Pentoxifylline on inflammatory burden, oxidative stress and platelet aggregability in hypertensive type 2 diabetes mellitus patients
(2007) Rituparna Maiti; N.K. Agrawal; D. Dash; B.L. Pandey
Objectives: Inflammation and oxidative stress are main culprits behind atherosclerosis in diabetes mellitus. This study explores the effect of add-on Pentoxifylline on inflammatory burden and oxidative stress in hypertensive diabetic patients. Research design and methods: 60 hypertensive type 2 diabetic, aged ≥ 45 years were evaluated for anthropometry, clinical parameters, C-reactive protein, total leukocyte count, erythrocyte sedimentation rate, serum albumin, plasma malondialdehyde, blood reduced glutathione, platelet aggregation and clot retraction profile. With informed consent and randomization, Pentoxifylline (400 mg) was prescribed to 30 patients orally twice daily with meals as add-on therapy to the standard therapeutic regimen for one month. The particular parameters were repeated in 26 patients in control group and 25 patients in Pentoxifylline group who completed the follow up. The study was a randomized, open, add-on clinical trial with parallel controls. Results: At one-month follow-up, in the Pentoxifylline group, there was 20.9% decrease (p < 0.001) in C-reactive protein, 18% reduction (p < 0.001) in erythrocyte sedimentation rate, 11.1% reduction (p < 0.001) in total leukocyte count and 5.8% increase (p = 0.003) in serum albumin. Pentoxifylline showed 20.2% reduction in plasma malondialdehyde and 4.6% increase in blood reduced glutathione level. In therapeutic dose range, Pentoxifylline exerted a significant anti-aggregatory effect and a dose dependent decrease in clot retraction in-vitro but there was no significant change in ex-vivo clot retraction. The control group showed no statistically significant change in parameters assessed. Conclusion: This study reveals improvements in inflammatory markers, oxidative stress and platelet-aggregation by Pentoxifylline, thus preventing atherosclerosis in diabetes mellitus. © 2007 Elsevier Inc. All rights reserved.
Effect of propranolol on platelet signal transduction
(Portland Press Ltd, 1995) D. Dash; K. Rao
Propranolol inhibits platelet secondary aggregation and secretion by mechanisms unrelated to its β-adrenergic-blocking activity. We previously reported that a major effect of the drug is perturbation of the physical microenvironment of the human platelet membrane. To explore further the molecular mechanisms underlying propranolol-mediated platelet inhibition, we studied protein kinase C activity, estimated from the phosphorylation of the substrate protein pleckstrin, in propranolol-treated human platelets. The drug inhibited activation of the enzyme in thrombin-stimulated platelets but not in platelets stimulated with phorbol esters, indicating that its site of action might be upstream of protein kinase C. It also inhibited the activity of phospholipase C, determined from the extent of generation of inositol phosphates and phosphatidic acid, in platelets stimulated with thrombin as well as the non-hydrolysable GTP analogue guanosine 5'-[β,γ-imido]triphosphate in a dose-dependent manner. These data suggest that propranolol inhibits signal transduction in thrombin-stimulated platelets by interacting at the level of phospholipase C and exclude interaction of the drug with the downstream effector enzyme protein kinase C.
Elevated plasminogen activator inhibitor type-1 (PAI-1) as contributing factor in pathogenesis of hypercoagulable state in antiphospholipid syndrome
(Springer Verlag, 2013) N.K. Singh; A. Gupta; Dibya R. Behera; D. Dash
The aim of this study is to explore the role of plasminogen activator inhibitor type 1 (PAI-1) in primary and secondary antiphospholipid syndrome (APS). Thirty patients of APS (24 primary and 6 secondary) were recruited in the study who fulfilled the revised Sapporo criteria. Control groups comprised of age- and sex-matched 10 healthy volunteers and 10 patients each of systemic lupus erythematosus and rheumatoid arthritis without any antecedent thrombotic event and/or APS-related pregnancy morbidity. Serum samples were tested for PAI-1 antigen levels measured by quantitative ELISA. Positivity rate of PAI-1 in patients of primary, secondary as well as total APS patients was significantly higher in relation to age- and sex-matched healthy volunteers (p = 0.010, p = 0.003 and p < 0.001, respectively). Mean ± SEM levels of PAI-1 in primary and secondary as well as total APS patients were significantly higher (p = 0.006, p < 0.001 and p < 0.001) in relation to healthy controls. Correlation of PAI-1 levels (mean ± SEM) with clinical characteristics, that is, thrombosis and pregnancy morbidity, revealed significantly higher levels of PAI-1 (p < 0.001) in patients having thrombosis and APS-related pregnancy morbidity. Elevated PAI-1 level leading to impaired fibrinolysis plays a significant role in producing hypercoagulable state in primary and secondary APS. © 2013 Springer-Verlag Berlin Heidelberg.
Enhanced photocatalytic degradation of dyes under sunlight using biocompatible TiO2 nanoparticles
(Institute of Physics Publishing, 2017) B. Bharati; A.K. Sonkar; N. Singh; D. Dash; Chandana Rath
As TiO2 is one of the most popular photocatalysts, we have studied here the photocatalytic degradation of the most common dyestuffs like rhodamine B (RhB), congo red (CR) and methylene blue (MB), which mainly come from the textile and photographic industries using nanoparticles of TiO2. Nanoparticles of TiO2 synthesized through a simple and cost effective sol-gel technique crystallizes in the anatase phase, showing a band gap less than that of bulk value. Particles consisting of coherently scattered domains of size 33 nm are found to be agglomerated and polycrystalline in nature. While the degradation rates of MB, CR and RhB after irradiating with a renewable source of energy, i.e. sunlight, show 100% degradation, TiO2 irradiated with UV light of 4.8 eV shows a much slower degradation rate. To use the waste water after photocatalysis, we examine further the biocompatibile nature of the TiO2 nanoparticles by platelet interaction activity, hemolysis effect and MTT assay. It is worth mentioning here that TiO2 nanoparticles are found to be highly hemocompatible, show no platelet aggregation, and the level of intracellular ROS in human platelets does not show significant change in ROS level. We conclude that TiO2 nanoparticles constitute an excellent photocatalyst and biocompatible material, and that after photocatalytic degradation of dye effluents obtained from textile industries, purified water can be used in agriculture and domestic sectors. © 2017 IOP Publishing Ltd.
Fetal growth in maternal anaemia
(Oxford University Press, 1997) P.N. Singla; M. Tyagi; Ashok Kumar; D. Dash; R. Shankar
The effect of maternal iron deficiency anemia on fetal growth was studied in 54 anaemic (haemoglobin < 11.0 g/dl) mothers. Twenty-two mothers served as controls (haemoglobin ≤ 11.0 g/dl). All the women had singleton live births at term gestation. The maternal iron status was assessed by serum ferritin estimation. The birth weight, head circumference, chest circumference, mid-arm circumference, and crown heel length were significantly low in infants born to women with moderate haemoglobin 6.1 ± 8.5 g/dl) and severe anaemia (haemoglobin ≤ 6.0 g/dl), in comparison to infants born to non-anaemic women. Similarly, birth weight, mid-arm circumference, and crown-heel length were significantly low in infants of women with depleted iron stores (serum ferritin < 10 μg/l) than in infants of women with serum ferritin levels of 20 μg/l or more. A indices of fetal growth showed linear relationships with maternal haemoglobin, as well as with serum ferritin. The growth retarding effect of maternal anaemia was more on fetal birth weight and mid-arm circumference than on other anthropometric indices of the newborn.
Fetal iron status in maternal anemia
(Blackwell Publishing Ltd, 1996) P.N. Singla; M. Tyagi; R. Shankar; D. Dash; A. Kumar
Hemoglobin, serum iron, transferrin saturation and ferritin were measured on paired maternal and cord blood samples in 54 anemic (hemoglobin < 110 g/L) and 22 non-anemic (hemoglobin ≤ 110 g/L) pregnant women at term gestation. The levels of hemoglobin, serum iron, transferrin saturation and ferritin were significantly low in the cord blood of anemic women, suggesting that iron supply to the fetus was reduced in maternal anemia. The linear relationships of these parameters with both maternal hemoglobin and maternal serum ferritin indicated that the fetus extracted iron in amounts proportional to the levels available in the mother. Infants of mothers with moderate and severe anemia had significantly lower cord serum ferritin levels and hence poor iron stores at birth. It is concluded that iron deficiency anemia during pregnancy adversely affects the iron endowment of the infant at birth.
Foreword
(Springer Singapore, 2022) D. Dash
[No abstract available]
Interconversion of tight and loose couple 50 S ribosomes and translocation in protein synthesis
(1985) D.P. Burma; A.K. Srivastava; S. Srivastava; D. Dash
[No abstract available]
Intranasal curcumin ameliorates airway inflammation and obstruction by regulating MAPKinase activation (p38, Erk and JNK) and prostaglandin D2 release in murine model of asthma
(Elsevier B.V., 2016) Subhashini; Preeti S. Chauhan; D. Dash; B.N. Paul; Rashmi Singh
Asthma, a multifactorial, chronic inflammatory disease encompasses multiple complex pathways releasing number of mediators by activated mast cells, eosinophils and T lymphocytes, leading to its severity. Presently available medications are associated with certain limitations, and hence, it is imperative to search for anti-inflammatory drug preferably targeting signaling cascades involved in inflammation thereby suppressing inflammatory mediators without any side effect. Curcumin, an anti-inflammatory molecule with potent anti-asthmatic potential has been found to suppress asthmatic features by inhibiting airway inflammation and bronchoconstriction if administered through nasal route. The present study provides new insight towards anti-asthmatic potential of intranasal curcumin at lower doses (2.5 and 5.0 mg/kg) in Balb/c mice sensitized and challenged with ovalbumin (OVA) which is effective in inhibiting airway inflammation. These investigations suggest that intranasal curcumin (2.5 and 5.0 mg/kg) regulates airway inflammation and airway obstruction mainly by modulating cytokine levels (IL-4, 5, IFN-y and TNF-α) and sPLA2 activity thereby inhibiting PGD2 release and COX-2 expression. Further, the suppression of p38 MAPK, ERK 42/44 and JNK54/56 activation elucidate the mechanism behind the inhibitory role of intranasal curcumin in asthma progression. Thus, curcumin could be better alternative for the development of nasal formulations and inhalers in near future. © 2015 Elsevier B.V. All rights reserved.