Subir Chandra Dasgupta

A high molecular weight protein Bengalin from the Indian black scorpion (Heterometrus bengalensis C.L. Koch) venom having antiosteoporosis activity in female albino rats

This study reports the presence of a high molecular weight protein (Bengalin) from the Indian black scorpion (Heterometrus bengalensis) venom having antiosteoporosis activity in experimental osteoporosis developed in female albino Wister rats. Bengalin was purified through DEAE-cellulose ion exchange chromatography and high performance liquid chromatography. The molecular weight of the Bengalin was found to be 72kDa and the first 20 amino acid sequence was found to be G-P-L-T-I-L-H-I-N-D-V-H-A-A/R-F-E-Q/G-F/G-N-T. Bengalin exhibited significant antiosteoporosis activity in experimental female rats, which was confirmed through analysis of urine Ca(2+), PO(4)(3-), CRE & OH-P. Bengalin (3 microg and 5 microg/100g rat/i.p.) antagonized osteoporosis by restoring urinary Ca(2+), PO(4)(3-), CRE and OH-P, serum/plasma Ca(2+), PO(4)(3-), ALP, TRAP, PTH, T(3), TSH, Osteocalcin, IL1, IL6 and TNF alpha and bone minerals Ca(2+), P, Mg(2+), Zn(2+), Na(+), as compared with the sham operated control rats. Bone minerals density of osteoporosis female rats was improved due to Bengalin, observed through DEXA scan. Subacute toxicity studies in male albino mice, Bengalin showed cardiotoxicity. In vivo experiments, Bengalin showed cardiotoxicity on isolated guinea pig heart, guinea pig auricle, and neurotoxicity on isolated rat phrenic nerve diaphragm preparation. Further detail studies on the toxicity, antiosteoporosis and structural identity of Bengalin are warranted.

A sleep inducing factor from common Indian toad (Bufo melanostictus, Schneider) skin extract.

Bufo melanostictus (common Indian toad) acquire different bioactive substances in their skin during their life-time in wide ecological habitat. Earlier investigation from this laboratory revealed that toad (B. melanostictus) skin extract (TSE) posses different bioactive compounds of different diversity (Das, M., Auddy, B. and Gomes, A., 1996. Pharmacological study of the toad skin extract on experimental animals. Indian J. Pharmacol. 28, 72-76). Among these sleep induction and sleep potentiation indicated the possibility of sleep inducing factor(s) in TSE. One such sleep inducing factor (SIF) was isolated and purified by neutral alumina column chromatography followed by HPLC. Spectroscopy (UV, IR, FAB-MASS) study indicated that the sleep inducing factor was a 880 Dalton conjugated aromatic compound with a hydroxyl and carbonyl functional group. Biological study showed that SIF produced no lethality in male albino mice upto the dose of 8 mg/kg, i.v. Cyproheptadine antagonised SIF induced contraction of isolated smooth muscle indicating histamine/serotonin receptor mediated action of SIF. EEG studies showed that SIF increased sleep and decreased awakening condition of freely moving rats. Biochemical studies showed that SIF produced significant alteration of brain biogenic amine levels, monoamine oxidase (MAO) and tryptophan hydroxylase (TH) activity. This may be the reason of SIF induced sleep, although the SIF induced sleep mechanism needs further detail investigation.

Protection against osteoarthritis in experimental animals by nanogold conjugated snake venom protein toxin gold nanoparticle-Naja kaouthia cytotoxin 1.

Background & objectives: Increased severity of osteoarthritis (OA) and adverse side effects of its treatment led to the search for alternative therapies. It was previously reported that snake venom protein toxin Naja kaouthia cytotoxin 1 (NKCT1) and gold nanoparticle (GNP) individually have potential against excremental arthritis. In this study, we analyzed the protective activity of GNP conjugated protein toxin NKCT1 (GNP-NKCT1) against experimental OA. Methods: Gold nanoparticle conjugation with NKCT1 (GNP-NKCT1) was done and its physiochemical properties were studied. OA was induced in male albino rats by intra-articular injection of bacterial collagenase and treatment was done with NKCT1/GNP-NKCT1/standard drug (indomethacin). Physical parameter (ankle diameter), urinary markers (hydroxyproline, glucosamine, pyridinoline, deoxypyridinoline), serum and synovial membrane pro-inflammatory markers [tumour necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), IL-17, vascular endothelial growth factor (VEGF)] and matrix metalloproteinase 1 (MMP1) were measured. Joint histopathology and scanning electron microscopy imaging of articular cartilage surface were also done. Results: Physical parameters, urinary markers, serum and synovial membrane pro-inflammatory makers and MMP1 were increased in arthritic rats and significantly restored after GNP-NKCT1/NKCT1 treatment. Joint histopathology and scanning electron microscopy imaging of articular cartilage surface also indicated the protective effect of GNP-NKCT1 against inflammatory response and cartilage degradation in osteoarthritic rats. Interpretation & conclusions: In this study restoration of the arthritic markers and bone degradation by GNP-NKCT1 treatment indicated the anti-osteoarthritic property of GNP-NKCT1. Further studies need to be done to confirm these findings.