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- 저자 : Iraj Khodadadi (검색결과 3 건)
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Vahid Khanjarsim,Jamshid Karimi,Iraj Khodadadi,Adel Mohammadalipour,Mohammad Taghi Goodarzi,Ghasem Solgi,Mohammad Hashemnia 전남대학교 의과학연구소 2017 전남의대학술지 Vol.53 No.2
Nilotinib as a tyrosine kinase inhibitor has been recently used to improve the liver fibrosis process, but the exact mechanisms still require further clarification. In this study, we investigated the anti-fibrotic effects of Nilotinib via RAGE/HMGB1axis and antioxidant mechanisms. This experimental study was performed in the Hamadan University of Medical Sciences, Iran, from May 2015 to December 2016. Liver fibrosis was induced in Wistar male rats by CCL4. Rats were gavaged daily with Nilotinib (10 mg/kg). RAGE, HMGB1, TNF-a and TGF-b mRNA expression were evaluated by quantitative RT-PCR. TNF-a protein levels were measured using the immunoassay method. Thiol groups, carbonyl groups, nitric oxide levels and glutathione peroxidase activity were measured by spectrophotometric methods.The results showed that Nilotinib decreased TNF-a, TGF-b, RAGE and HMGB1 mRNA expression (p<0.001) in the liver tissues of the fibrosis group. Nilotinib also decreased carbonyl groups and nitric oxide levels and increased thiol groups and glutathione peroxidase activity in the fibrosis groups. The histopathological changes were found to be attenuated by Nilotinib. In conclusion, Nilotinib can improve liver fibrosis and open new mechanisms of the anti-fibrotic properties of Nilotinib.
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Circulating Betatrophin Levels Are Associated with the Lipid Profile in Type 2 Diabetes
Hassan Ghasemi,Heidar Tavilani,Iraj Khodadadi,Massoud Saidijam,Jamshid Karimi 전남대학교 의과학연구소 2015 전남의대학술지 Vol.51 No.3
Betatrophin is a newly characterized circulating hormone that is produced in tissuessuch as adipose tissue and liver and stimulates pancreatic beta-cell proliferation. Thepurpose of the current study was to examine circulating betatrophin levels in Iranianpatients with type 2 diabetes mellitus (T2DM) and in normal controls. Seventy-five subjectswere enrolled in this case-control study in the following two groups: T2DM patients(n=40) and a group of age-, sex-, and BMI-matched normal control subjects (n=35). Circulating betatrophin concentrations as well as the blood lipid profile, body mass index(BMI), fasting blood sugar (FBS), glycated hemoglobin (HbA1c), and insulin resistancewere determined. Circulating betatrophin levels were significantly higher in patientswith T2DM than in the normal subjects (4.79±1.53 ng/mL vs. 2.79±1.11 ng/mLrespectively; p=0.001). Serum triacylglycerol and total cholesterol were also significantlyhigher in patients with T2DM than in the control group. In the patients withT2DM, serum betatrophin was positively correlated with age, FBS, TG, total cholesterol,and HbA1c. The results of this initial study in Iran have shown that circulating betatrophinlevels are significantly increased in Iranian patients with T2DM comparedwith a control group. Additionally, it is postulated that betatrophin as a novel hormonemay be involved in the generation of an atherogenic lipid profile.
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Ashkan Karbasi,Ali Abbasi,Abbas Mohagheghi,Jalal Poorolajal,Farzad Emami,Shirin Moradkhani,Iraj Khodadadi,Mahmoud Gholyaf,Heidar Tavilani 전남대학교 의과학연구소 2024 전남의대학술지 Vol.60 No.1
Contrast-induced acute kidney injury (CI-AKI) is a frequent challenge following the injection of contrast media and its subsequent oxidative stress. The aim of the present study was to evaluate the preventive effects of coenzyme Q10 (Q10), as a mitochondrial-targeted antioxidant in CI-AKI in diabetic patients, who account for a large proportion of angiographic cases. A total of 118 diabetic patients were randomly assigned to receive 120 mg of oral coenzyme Q10 (Q10 group) or placebo (Placebo group) for four days, starting 24 hours before contrast media injection. Blood urea nitrogen (BUN), serum and urinary creatinine, estimated glomerular filtration rate (eGFR), urinary malondialdehyde (UMDA), urinary total antioxidant capacity (UTAC), and urinary mitochondrial to nuclearDNA ratios (mtDNA/nDNA ratio) were evaluated before and after the treatment period. Urine sediments were also evaluated to report the urine microscopy score (UMS).The levels of BUN, serum and urine creatinine, and UMS were similar in the Q10 and placebo groups. EGFR was lower in the Q10 group before the treatment (p=0.013) but not after. The urinary mtDNA/nDNA ratio was 3.05±1.68 and 3.69±2.58 in placebo and Q10 groups, but UTAC was found to be lower in Q10 both before (p=0.006) and after the treatment (p<0.001). The incidence of CI-AKI was 14.40% and the mtDNA/nNDA ratio was similar between CI-AKI and non-CI-AKI patients. In conclusion, Q10 treatment shows no favorable effect on prevention of CI-AKI or a urinary mtDNA/nDNA ratio among diabetic patients.
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