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.
Objective: To study the Inhibition of proteasome activity by the dietary flavonoid Quercetin associated with growth inhibition in cultured breast cancer cells and xenografts. Methods: MCF-7 breast cancer cell cultures and xenografts were treated with quercetin, carried out by following measurement of reduced cellular viability/proliferation, proteasome inhibition, and apoptosis induction. Inhibition of the proteasome was decided by levels of the proteasomal chymotrypsin-like activity, by target proteins, and by accumulation of proteasome target proteins in extracts of the treated cells or tumours. Apoptotic cell inhibition was measured by capase-3/caspase-7 activation, poly (ADP-ribose) polymerase cleavage, and immunohistochemistry for terminal nucleotidyl transferase. Results: This result is carried out for the first time by us that quercetin inhibits the proteasomal chymotrypsin-like activity and induces apoptosis not only in cultured MCF-7 cell lines but also in MCF-7 xenografts moreover, while quercetin has antibreast tumour activity and no toxicity was observed to the tested animals. Conclusion: We have shown that quercetin is an effective proteasome inhibitor in cultured breast cancer cells and in breast cancer xenografts. Furthermore, quercetin induces apoptotic cell death in human breast cancer cells and exhibits anticancer activities in tumours. The results suggest its potential benefits in breast cancer prevention and treatment.
Introduction: Traditional medicines for mammary tumour are unreasonable and have genuine symptoms. Non-ordinary normal medications have increased wide acknowledgment because of their assurance of a cure with negligible or no symptoms, however minimal experimental confirmation exists. One such basic cure is the leaves of the Euphorbia hirta plant. Methods: It is initially reported utilization of the fluid concentrate of Euphorbia hirta leaves breast cancer cells. The capacity of the concentrate to impel apoptosis and corruption in the human bosom malignancy cell line MCF-7, contrasted with typical human skin fibroblasts (MDA MB-231), was dictated by morphological changes in the cells utilizing light microscopy, DNA fragmentation, and brilliant stains (Annexin V and Propidium Iodide) utilizing Flow Cytometry and fluorescent microscopy. Results: Apoptosis was instigated in both cells, and more in MCF-7, when they were treated with 25% and half concentrate, while rot was watched mostly after presentation to raised concentrate fixations (75%). DNA discontinuity came about for both cells, in a period and dosage subordinate way. Both cells, at all concentrate fixations, demonstrated no critical contrasts in the quantity of living, dead, apoptotic, and necrotic cells. Conclusion: At long last, the outcomes might show that apoptotic changes in MCF-7 might be free of caspase-3, which is included in apoptosis and is inadequate in MCF-7 cells.
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