@article {505, title = {Pharmacognostic Evaluation of Curcumin on Diabetic Retinopathy in Alloxan-induced Diabetes through NF-KB and Brn3a Related Mechanism}, journal = {Pharmacognosy Journal}, volume = {10}, year = {2018}, month = {January 2018}, pages = {324-332}, type = {Original Article}, chapter = {324}, abstract = {

Background: Diabetic retinopathy is one of the most common micro vascular complication of diabetes and involves an abnormal pathology of major retinal pigment epithelium, inter retinal oedema and intraocular neovascularisation where pro-inflammatory proteins including ICAM-1,iNOS and VEGF release by activation of enzyme CaMKII/NF-kB expression Diabetic induced oxidative stress followed by deactivation of Brn3a expression in the retinal ganglionic cells are also early events in pathogenesis of Diabetic retinopathy. These factors are important contributors to the development of clinically significant diabetic retinopathy. Objective: Objective of this study to examine the effect of curcumin with antioxidant and anti-inflammatory properties obtained from Curcuma longa against diabetes-induced retinal vascular damage and its mechanism of action by in-vivo in retinas of rat rendered diabetic by alloxan and in vitro in western blotting and RGC tissue culture. Method: We administered curcumin or saline vehicle to experimental animals daily for 12 weeks. Vascular permeability, expression of CaMK II/NF-kB, Retinal morphology and neuropathic change of the retinal ganglion cells were investigated. Results: As an anti-oxidant, curcumin raised Retinal Ganglionic cells by increasing Brn3a expression during oxidative stress condition and subsequently decreased the expression of inflammatory mediators such as VEGF, iNOS and ICAM-1 as an anti-inflammatory agent by inhibiting CaMKII and NF-kB expression. Conclusion: Curcumin, a common food additive has beneficial effects in experimental studies of diseases that are characterised by increased oxidative stress and inflammatory reactions. It appears to be a useful adjunct therapy to possibly inhibit the progression of retinopathy, sight threatening complication faced by diabetic patients.

}, keywords = {Brn3a, CaKMII, Curcumin, Inflammation, NF-KB, Oxidative stress}, doi = {10.5530/pj.2018.2.56}, url = {http://fulltxt.org/article/486}, author = {Debasish Pradhan and Toffa Dasmohapatra and Gitanjali Tripathy} } @article {117, title = {Inhibition of MDR1 in mammary cell carcinoma reverses Multidrug Resistance by SOCS1}, journal = {Pharmacognosy Journal}, volume = {8}, year = {2016}, month = {09/2015}, pages = {103-112}, type = {Original Article}, chapter = {103}, abstract = {

Introduction: Suppressors of cytokine signalling (SOCS1), a newly indentified antiapoptotic molecule is a downstream effector of the receptor tyrosine kinase-Ras signalling pathway. Current study has uncovered that SOCS1 may have wide and imperative capacities, particularly because of its close correlation with malignant tumors. Methods: To investigate the impact of SOCS1 on MDR, we analyzed the expression of P-gp and SOCS1 by immunohistochemistry and found there was positive correlation between them. At that point we effectively interfered with RNA translation by the contamination of siRNA of SOCS1 into MCF7/ ADM breast cancer cell lines through a lentivirus, and the expression of the target gene was significantly inhibited. Results: After RNAi the drug resistance was reduced altogether and the expression of MDR1 mRNA and P-gp in MCF7/ADM cell lines demonstrated a significant decrease. Likewise the expression of P53 protein increased in a statistically significant manner (p\≤0.01) after RNAi exposure. Moreover, flow cytometry analysis uncovers that cell cycle and anti-apoptotic enhancing capacity of cells changed after RNAi treatment. Conclusion: These outcomes proposed SOCS1 may take part in breast cancer MDR by managing MDR1 and P53 expression, changing cell cycle and enhancing the anti-apoptotic ability of cells.

}, keywords = {Breast cancer, MDR1gene, Multidrug resistance, RNA interference., SOCS1 gene}, doi = {10.5530/pj.2016.2.2}, author = {Debasish Pradhan and Gitanjali Tripathy and Rakesh Kumar Pradhan and Shaktiprasad Pradhan and Soumyashree Rupambika Moharana} }