Soliman, Nema Ali;Zineldeen, Doaa Hussein;El-Khadrawy, Osama Helmy
Asian Pacific Journal of Cancer Prevention
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제15권2호
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pp.837-845
/
2014
Background: Overweight and obesity are recognized as major drivers of cancers including breast cancer. Several cytokines, including interleukin-6 (IL-6), IL-10 and lipocalin 2 (LCN2), as well as dysregulated cell cycle proteins are implicated in breast carcinogenesis. The nuclear, casein kinase and cyclin-dependent kinase substrate-1 (NUCKS-1), is a nuclear DNA-binding protein that has been implicated in several human cancers, including breast cancer. Objectives: The present study was conducted to evaluate NUCKS-1 mRNA expression in breast tissue from obese patients with and without breast cancer and lean controls. NUCKS-1 expression was correlated to cytokine profiles as prognostic and monitoring tools for breast cancer, providing a molecular basis for a causal link between obesity and risk. Materials and Methods: This study included 39 females with breast cancer (G III) that was furtherly subdivided into two subgroups according to cancer grading (G IIIa and G IIIb) and 10 control obese females (G II) in addition to 10 age-matched healthy lean controls (G I). NUCKS-1 expression was studied in breast tissue biopsies by means of real-time PCR (RT-PCR). Serum cytokine profiles were determined by immunoassay. Lipid profiles and glycemic status as well as anthropometric measures were also recorded for all participants. Results: IL-6, IL-12 and LCN2 were significantly higher in control obese and breast cancer group than their relevant lean controls (p<0.05), while NUCKS-1 mRNA expression was significantly higher in the breast cancer group compared to the other groups (p<0.05). Significant higher levels of IL-6, IL-12, and LCN2 as well as NUCKS-1 mRNA levels were reported in G IIIb than G IIIa, and positively correlated with obesity markers in all obese patients. Conclusions: Evaluation of cytokine levels as well as related gene expression may provide a new tool for understanding interactions for three axes of carcinogenesis, innate immunity, inflammation and cell cycling, and hope for new strategies of management.
The Framingham risk score (FRS) has been used to assess the risk of a cardiovascular event and to identify patients for risk factor modifications. Therefore, the purpose of this study was to evaluate the relationship of the FRS with dietary intake and inflammatory biomarkers. We conducted a cross-sectional study of 180 men ($49.2{\pm}10.2$ years) with MS. Serum levels of high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), and adiponectin were examined. Participants were asked to complete the food frequency questionnaire (FFQ) using the previous 1 year as a reference point. The absolute cardiovascular disease (CVD) risk percentage over 10 years was calculated to estimate the FRS, which was classified as low risk (< 10%), intermediate risk (10-20%), and high risk (> 20%). Mean intake of polyunsaturated fatty acids was lower in subjects who had > 20% FRS than in subjects who had < 10% FRS ($3.7{\pm}1.9$ g/day vs. $4.7{\pm}1.9$ g/day; P < 0.05). Significant differences in the Index of Nutritional Quality of protein, phosphorus, iron, vitamin A, vitamin $B_1$, niacin, vitamin $B_6$, and vitamin C were observed between the > 20% FRS group and the < 10% FRS group (P < 0.05). IL-6 concentrations were significantly lower in subjects with a < 10% FRS than in subjects who were 10-20% FRS or > 20% FRS ($0.91{\pm}0.26$ vs. $1.48{\pm}033$ vs. $2.72{\pm}0.57$ pg/mL, respectively; P < 0.05). IL-6 and dietary intake of polyunsaturated fatty acids together explained 6.6% of the variation in FRS levels in a stepwise multiple regression model. Our results provide some evidence that dietary intake in the higher CVD risk group was inferior to that in the lower risk group and that dietary fat intake and IL-6 were associated with FRS and MS in Korean men.
Epilepsy is a chronic disease occurring in approximately 1.0% of the world's population. About 30% of the epileptic patients treated with availably antiepileptic drugs (AEDs) continue to have seizures and are considered therapy-resistant or refractory patients. The ultimate goal for the use of AEDs is complete cessation of seizures without side effects. Because of a narrow therapeutic index of AEDs, a complete understanding of its clinical pharmacokinetics is essential for understanding of the pharmacodynamics of these drugs. These drug concentrations in biological fluids serve as surrogate markers and can be used to guide or target drug dosing. Because early studies demonstrated clinical and/or electroencephalographic correlations with serum concentrations of several AEDs, It has been almost 50 years since clinicians started using plasma concentrations of AEDs to optimize pharmacotherapy in patients with epilepsy. Therefore, validated analytical method for concentrations of AEDs in biological fluids is a necessity in order to explore pharmacokinetics, bioequivalence and TDM in various clinical situations. There are hundreds of published articles on the analysis of specific AEDs by a wide variety of analytical methods in biological samples have appears over the past decade. This review intends to provide an updated, concise overview on the modern method development for monitoring AEDs for pharmacokinetic studies, bioequivalence and therapeutic drug monitoring.
Misaengtang (MST), a formula of Korean herbal medicines, has been used as a weight-controlling recipe. We have investigated two experiment of body weight regulation by MST In rats. i) The anti-obesity effect of MTS on a high fat diet-induced obesity, male Sprague-Dawley rats were fed with a high-fat diet containing 30% in the absence or presence of MST (0.3, 1 or 3%) or a reference orlistat (0.05%) for 6 weeks. ii) weight-decrease effect of MST on normal diet, same animal were fed with a normal diet in the absence or presence of MST (3%) for 6 weeks. And the body weights, daily feed and water consumptions, organ weights, fat weights serum biochemistry were measured. In both experiments, MST and orlistat did not affect the body weight gain. But orlistat significantly increased the feed and water consumptions, leading to low-feed efficiency, and orlistat markedly reduced abdominal, paratesticular and perirenal fat weights, although increased the kidney weights. In MST, low dose (0.3%) of MST decreased the perirenal fat and increased the kidney weights in rats fed HFD, and MST 3% decreased the abdominal fat weights in rats fed normal diet. In addition, Orlistat caused changes in parameters of hepatotoxicity (AST and glucose), nephrotoxicity (BUN and B/C ratio) and lipid metabolism (HDL and triglycerides). In comparison, MST decreased AST, ALP and ALT, the hepatotoxicity markers, and somewhat improved the hepatic fatty degeneration. Taken together, it is suggested that MST does not exert anti-obesity activity as well as remarkably direct effects, but MST may be potentially benefit for dietary cure and exercise-cure of obesity.
Raphanus sativus (Cruciferaceae), commonly known as radish is widely available throughout the world. From antiquity it has been used in folk medicine as a natural drug against many toxicants. The present study was designed to evaluate the hepatoprotective activity of radish (Raphanus sativus) enzyme extract (REE) in vitro and in vivo test. The $IC_{50}$ values of REE in human liver derived HepG2 cells was over 5,000 ${\mu}g/ml$ in tested maximum concentration. The effect of REE to protect tacrine-induced cytotoxicity in HepG2 cells was evaluated by MTT assay. REE showed their hepatoprotective activities on tacrine-induced cytotoxicity and the $EC_{50}$ value was 1,250 ${\mu}g/ml$. Silymarin, an antihepatotoxic agent used as a positive control exhibited 59.7% hepatoprotective activity at 100 ${\mu}g/ml$. Moreover, we tested the effect of REE on carbon tetrachloride ($CCl_4$)-induced liver toxicity in rats. REE at dose of 50 and 100 mg/kg and silymarin at dose of 50 mg/kg were orally administered to $CCl_4$-treated rats. The results showed that REE and silymarin significantly reduced the elevated levels of serum enzyme markers induced by $CCl_4$. The biochemical data were supported by evaluation with liver histopathology. These findings suggest that REE, can significantly diminish hepatic damage by toxic agent such as tacrine or $CCl_4$.
Atopic dermatitis (AD) is an inflammatory skin disease commonly characterized by infiltration of inflammatory cells into skin lesions. Keratinocytes produce many chemokines that are involved in the pathogenesis of skin disorders. In particular, macrophage-derived chemokine (MDC/CCL22) and thymus and activationregulated chemokine (TARC/CCL17) are Th2-type cytokines. Serum MDC and TARC levels are increased in AD patients. In this study, we investigated the anti-inflammatory effect and mechanism of action of the active fraction from Prunus yedoensis bark. We evaluated their inhibitory effects on the AD-like inflammatory markers (MDC and TARC) and JAK-STAT pathway (STAT1) in HaCaT keratinocytes. The EtOAc fraction of the crude extract (80% EtOH) and the E5 sub-fraction potently inhibited the induction of MDC and TARC mRNA and protein at 50 ${\mu}g$/mL in HaCaT cells. In addition, the E5 sub-fraction inhibited the phosphorylation of STAT1 protein associated with IFN-$\gamma$ signaling transduction in a dose-dependent manner. Thus, P. yedoensis may have antiatopic activity by suppressing the inflammatory chemokines (MDC and TARC).
An extract of Allomyrina dichotoma larva (ADL), one of the insects used most frequently in traditional Chinese medicine for the treatment of liver diseases such as hepatocirrhosis and hepatofibrosis, was assessed for antioxidant bioactivity in this study. In the current work, we have investigated the protective effects of ADL extracts on tert-butyl hydroperoxide (t-BHP)-induced hepatotoxicity in cultured hepa1c1c7 cells and in the mouse liver. The treatment of the hepa1c1c7 cells with ADL extracts induced a significant reduction of t-BHP-induced oxidative injuries, as determined by cell cytotoxicity, lipid peroxidation (LPO) and reactive oxygen species contents, in a dose-dependent manner. Moreover, ADL extracts evidenced a protective effect against t-BHPinduced oxidative DNA damage, as revealed by the results of the Comet assay in hepa1c1c7 cells. ADL extracts also protected against hydroxyl radical-induced 2-deoxy-d-ribose degradation by ferric ion-nitrilotriacetic acid and $H_2O_2$. In addition, ADL extracts were shown to be able to quench 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radicals. Our in vivo study revealed that ADL extracts pretreatment applied prior to t-BHP administration significantly prevented an increase in the serum levels of hepatic enzyme markers and reduced LPO in the mouse liver in a dose-dependent manner. Taken together, these results suggest that the protective effects of ADL extracts against t-BHP-induced hepatotoxicity may be attributable, at least in part, to its ability to scavenge free oxygen radicals, and to protect against DNA damage due to oxidative stress.
We exposed ICR mice to low-dose (0.2 Gy) and low-dose-rate (0.7 mGy/h) $\gamma$-radiation ($^{137}Cs$) in the Low-dose-rate Irradiation Facility at the Radiation Health Research Institute to evaluate systemic effects of low-dose radiation. We compared the body and organ weights, number of blood cells (white and red blood cells and platelets), levels of biochemical markers in serum, and frequency of micronuclei in polychromatic erythrocytes between low-dose irradiated and non-irradiated control mice. The ICR mice irradiated with total doses of 0.2 and 2 Gy showed no changes in body and organ weights, number of blood cells (white and red blood cells), or frequency of micronuclei in the polychromatic erythrocytes of peripheral blood. However, the number of platelets (P = 0.002) and the liver weight (P < 0.01) were significantly increased in mice exposed to 0.2 and 2 Gy, respectively. These results suggest that a low-dose-rate of 0.7 mGy/h does not induce systemic damage. This dose promotes hematopoiesis in the bone marrow microenvironment and the proliferation of liver cells. In the future, the molecular biological effects of lower doses and dose rates need to be evaluated.
Background: Black ginseng has a more potent biological activity than non-steamed ginseng. We investigated the effects of long-term intake of dietary black ginseng extract (BG) on antioxidant activity in aged mice. We also compared the effects of BG on cognitive deficits with those of white ginseng extract (WG) and red ginseng extract (RG). Methods: Ten-month-old mice were fed an AIN-93G-based diet containing 10 g/kg (low dose, L) or 30 g/kg (high dose, H) WG powder, RG powder, or BG powder for 24 wk. We measured serum lipids, the activities of antioxidant enzymes, and malondialdehyde levels. Additionally, the protein expression levels of choline acetyltransferase and vesicular acetylcholine transporter, which are presynaptic cholinergic markers in the cortex and hippocampus of the brain, were measured by western blotting. Results: Triglyceride levels were reduced in all the extract-treated mice, except those in the LBG group. High-density lipoprotein cholesterol levels in the HBG group were higher than those in the control group. Total cholesterol levels were reduced in the LBG group. Additionally, glucose levels in the HBG group were significantly reduced by 41.2%. There were lower levels of malondialdehyde in the LBG group than in the control group. Furthermore, glutathione reductase activity increased in the HWG group and the HRG group. The protein expression levels of choline acetyltransferase and vesicular acetylcholine transporter significantly increased in all the ginseng-treated groups. Conclusion: The results suggest that supplementation with the tested ginseng extracts may suppress the cognitive decline associated with aging, via regulation of the cholinergic and antioxidant defense systems.
Nam, Yoonjin;Bae, Jinhyung;Jeong, Ji Hoon;Ko, Sung Kwon;Sohn, Uy Dong
Journal of Ginseng Research
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제42권4호
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pp.540-548
/
2018
Background: Acute hepatic failure is a life-threatening critical condition associated with rapid deterioration of liver function and liver transplantation. Several studies have shown that Panax ginseng Mayer has antidiabetic and hepatoprotective effects. However, the hepatoprotective effect of ginseng berry is still unveiled. In this study, we evaluated the hepatoprotective effects of ultrasonication-processed ginseng berry extract (UGBE) on acute hepatic failure model in rats. Methods: Ginseng berry extract (GBE) was ultrasonically processed. The GBE, silymarin, and UGBE were orally administered to male Sprague-Dawley rats for 4 wk. Twenty-four h after the last administration, rats were challenged with D-galactosamine (D-GalN)/lipopolysaccharide (LPS). Results: After ultrasonication, the component ratio of ginsenosides Rg2, Rg3, Rh1, Rh4, Rk1, Rk3, and F4 in GBE had been elevated. Administration of UGBE significantly increased the survival rate of D-GalN/LPS-challenged rats. Pretreatment with UGBE significantly decreased serum alanine aminotransferase, aspartate aminotransferase, and total bilirubin levels in D-GalN/LPS-challenged rats in a dose-dependent manner. The levels of enzymatic markers for oxidative stress (superoxide dismutase, glutathione peroxidase, catalase, and glutathione) were increased by UGBE treatment in a dose-dependent manner. Tumor necrosis factor alphalevel, inducible nitric oxide synthase activities, and nitric oxide productions were reduced by UGBE treatment. In addition, hemeoxygenase-1 levels in liver were also significantly increased in the UGBE-treated group. The protein expression of toll-like receptor 4 was decreased by UGBE administration. Hematoxylin and eosin staining results also supported the results of this study showing normal appearance of liver histopathology in the UGBE-treated group. Conclusion: UGBE showed a great hepatoprotective effect on D-GalN/LPS-challenged rats via the toll-like receptor 4 signaling pathway.
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