Current Issue : April - June Volume : 2017 Issue Number : 2 Articles : 7 Articles
Background.Our aimwas to evaluate the protective effect of lipoic acid (LA) on fetal outcomeof diabeticmothers. Methods. Diabetes\nwas induced in female rats using streptozotocin and rats were made pregnant. Pregnant control (group 1;...
The present work aimed to evaluate the antiviral potential of Egyptian bee venom and honey bee derivatives namely phospholipase A2 (PLA2) and propolis against DNA and RNA virus models; HSV-1and RVFV. MTT assay was used to evaluate the cytotoxic effects of BV, PLA2 and propolis. Results showed that the tested BV, PLA-2 and propolis have cytotoxic effect on normal vero cell line and the cytotoxic effect was a concentration dependent and the calculated IC50 values were arranged in the order of EBV > PLA2 > propolis and the IC50 was 13.7, 25 and 30.8 µgm/ml respectively. The tested products showed antiviral potential against DNA and RNA virus models; HSV-1 and RVFV with a growth inhibition of 10 %, 10 % and 26.3 % for PLA2, EBV and propolis respectively in case of testing direct effect of HSV-1. In addition, in case of evaluation the inhibitory effect against RVFV as RNA virus model the inhibition was 7.7 %, 27 % and 15.4% post treatment with propolis, EBV and PLA2 respectively. The antiviral activity 1 hour infection pretreatment (indirect effect), the growth inhibition was in the order of 0 %, 21% and 26% for propolis, EBV and phospholipase in case of HSV-1virus. While in the RNA model, it was 33.3 %, 21 % and 0 % post treatment with propolis, EBV and PLA2 respectively. Data assure that there is difference in antiviral activity between bee products against both DNA and RNA virus. It was showed that propolis have direct effect on HSV-1 virus and indirect effect on RVFV virus. EBV show indirect antiviral effect on HSV-1 in addition to direct and indirect effect on RVFV. On the other hand, PLA2 show both indirect and direct effect on HSV-1 and only direct effect on RVFV virus....
This study aimed at estimating the anti-cancer potentials of Propolis, Egyptian bee venom on the colorectal cancer cell line HCT-116. The Egyptian bee venom showed higher toxicity on cells. After 24 hrs post treatment with Egyptian bee venom, mellitin, honey and propolis affected HCT-116 cells viability in a dose dependent manner. Our data showed a significant inhibitory effect on cells proliferation accompanied with some morphological changes. Also, up regulation of both P53 and Bax accompanied with down regulation of Bcl-2 were detected after 24 hrs post cellular treatment. Data recorded revealed that treatment with bee venom, mellitin, honey and propolis in addition to cisplatin showed clear anticancer potentials based on the up / down regulation of pro-apoptotic and anti-apoptotic genes. By bee venom, mellitin, honey and propolis induced apoptosis in HCT-116 cells which might be related to a mitochondrial-dependent pathway....
The number of studies on possible pharmacokinetic interactions between opioid\nanalgesics and nonsteroidal anti-inflammatory drugs (NSAIDs), which are commonly\nused in combination for the treatment of chronic pain, is limited. In rats, the\nmajor metabolic pathway of morphine is glucuronidation to morphine-3-glucuronide\n(M3G) by UDP-glucuronosyltransferase. In this study, we investigated the influence\nof diclofenac (NSAID) on the formation of M3G in vitro using rat liver tissue homogenates.\nCompetitive inhibition of M3G formation by diclofenac was observed with\nan average Ki of 19.9 �¼M. Because these in vitro findings suggested that a pharmacokinetic\ninteraction occurs in vivo , we investigated whether diclofenac inhibits the\nglucuronidation of morphine in rats. A single dose of diclofenac increased serum\nconcentrations of both morphine and M3G and showed a higher analgesic efficacy in\nthe Von Frey test. Furthermore, diclofenac caused a net decrease in morphine urine\nconcentrations, but the excretion of M3G through biliary and urinary routes was\nunchanged. These results demonstrated that in contrast to in vitro data a single dose\nof diclofenac did not alter the glucuronidation of morphine in vivo....
Diabetes is a chronic metabolic disorder that continues to present as a major health problem worldwide. It is the\nmajor cause of chronic kidney disease which in turn may lead to end-stage renal disease (ESRD) ending up in dialysis. Diabetic\nnephropathy (DN) is characterized by the development of overt proteinuria, increasing systemic blood pressure and declining\nrenal function. Various risk factors are involved in the development and progression of DN, among them hyperglycemia and\narterial hypertension are the major contributor. Hyperglycemia induced metabolic and hemodynamic pathways are proven to\nbe the mediators of kidney disease. Hyperglycemia causes the formation of Amadori products, which are the altered proteins\nand advanced glycation end products (AGE) are the molecular players in the phases of DN. Hemodynamic changes, hypertrophy,\nextracellular matrix accumulation, growth factor/cytokine induction, ROS formation, podocyte damage, proteinuria and\ninterstitial inflammation are the steps in the advancement of DN. Recent studies examining the pathogenesis of diabetic\ncomplications have focused on the complex interaction between genetic and hemodynamic mechanisms in addition to metabolic\nfactors such as advanced glycation, protein kinase C (PKC) activation and polyol production. The importance of the various\ncomponents, particularly with regard to the progression of DN, is currently being explored with the assistance of targeted drug\nintervention studies....
Oxidative stress and mitochondrial dysfunction are major events leading to nerve cell death. Oxidative stress and related mitochondrial dysfunction is one of the common cooperative sharing pathways involved in neurodegenerative disorders including Huntington's disease. Flavonoids have well known antioxidant activity. Diosmin is a flavone, a member of the flavonoid family, resemble the structure of oestrogen and display agonistic interactions with the oestrogen receptor. Oestrogen and diosmin is reported to be a neuroprotective antioxidant. Systemic 3-nitropropionic acid (10 mg/kg/i.p) treatment for 14 days in rats significantly induced huntington’s disease like symptoms in rats as indicated by reduced locomotor activity, body weight, grip strength, cognition, oxidative defense and mitochondrial enzymes (complex-I, -II and lactate dehydrogenase) activities in striatum. The effect of diosmin on 3 nitropropionic acid oxidative stress and mitochondrial enzyme activities was investigated. Treatment with diosmin (5, 10 and 15 mg/kg/oral) significantly reversed behavioral, biochemical enzyme dysfunctions in 3-nitropropionic acid treated group....
Prostate and colon cancer represent a major health problem worldwide. In the present study, we evaluated the anticancer\nproperties and cytotoxicity of Cerastes-cerastes (CC) snake venom on colon (Caco-2) and prostate (PC-3) cancer cells\nafter their pretreatment with variable concentrations of Bacillus Calmette-Gu�©rin (BCG) derived purified protein derivative\n(PPD). We monitoned the cell cycle arrest profile and specific cellular apoptosis markers (i.e. pro- and anti-apoptotic genes P53,\nBax and Bcl-2 in CC- and BCG/PPD-pretreated cells using real time PCR. The cytotoxicity was determined by using MTT assay.\nOur data show that 24 h-treatment of cancer cells with CC venom induced a concentration-dependent cytotoxicity with IC50\nvalues of 60 (Caco-2 cells) and 81 (PC-3 cells) �¼g/ml. Interestingly, addition of BCG/PPD at 25 and 50 �¼g/ml markedly increased\nthe CC venom-induced toxicity on cancer cells, with IC50 values of 1.04 and 0.59 �¼g/ml for Caco-2 (up to 102-fold increase) or\n2.78 and 0.70 �¼g/ml for PC-3 cells (up to 116-fold increase). By analyzing the cell cycle arrest and related gene expression\npattern, the main phase of cell cycle arrest was found to be G2/M in both cell lines. An S-phase arrest was also observed in PPD\npretreated colon Caco-2 cell line to a greater extent than that observed in cells only treated with CC venom. Up regulation of proapoptotic\nand down regulation of anti-apoptotic genes in PPD pretreated cells were significantly enhanced as compared to cells\ntreated with CC venom alone. In this study, we suggest that PPD -via its synergistic action with the CC venom-might be used as\nan enhancer of the anti-cancer properties of CC venom....
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