چکیده (انگلیسی):

Background and purpose: The 6th edition of International Diabetes Federation, 2014
shows an estimate of 387 million people with Type 2 diabetes mellitus (T2DM) worldwide, expected
to rise to 592 million by 2035. T2DM is a metabolic disorder, one of the reasons being oxidative
stress due to impairment in antioxidant enzymes. It leads to several complications such as micro
and macrovascular diseases. Cyclooxygenase1 (COX1) enzyme is the rate limiting factor for the
arachidonic pathway leading to vascular wall contraction with angiotensin II occurring in heart diseases
resulting from T2DM. COX1 determines 6-Keto Prostaglandin F1a (6-k-PGF1a) level, plays a
major role in vasodilation and restricts macrophage platelet aggregation. The aim of the present
study was to compare the COX1 expression and level of reactive oxygen species (ROS) in T2DM
patients and controls at different time periods in human macrophages in order to find a biomarker
or drug target.
Subjects and methods: The study subjects consisted of 100 individuals, 50 each from T2DM
patients and healthy sex/age matched controls. Cell proliferation by 3-(4,5-dimethylthiazol-2-yl)-2
,5-diphenyltetrazolium bromide (MTT) assay and ROS measurement by 20,70-dichlorofluorescein
diacetate (DCFDA) staining were performed at different time periods (24, 48, 72 h). COX1
mRNA expression was checked by relative quantification method after real-time polymerase chain
reaction (RT-PCR).
Results: The MTT assay showed that cell viability was significantly higher at 48 h (P< 0.05).
ROS production was found to be lowest at 24 h by DCFDA staining. ROS levels were raised in
T2DM patients as compared to controls. The quantitative RT-PCR analysis showed that the
COX1 expression was higher in T2DM patients as compared to healthy controls although not
significant (P > 0.05).