INHALATION EXPOSURE TO CIGARETTE SMOKE INDUCES ENDOTHELIAL NITRIC OXIDE SYNTHASE UNCOUPLING AND ENHANCES VASCULAR COLLAGEN DEPOSITION IN STREPTOZOTOCIN-INDUCED DIABETIC RATS

Session Name
HUMAN FACTOR IN THE USE OF DIABETES TECHNOLOGY
Session Type
E-POSTER VIEWING (EXHIBITION HOURS)
Date
20.02.2020, Thursday
Session Time
09:30 - 15:30
Channel
E-Poster Area
Lecture Time
09:52 - 09:53
Presenter
  • MOO-YEOL Lee, Korea, Republic of
Authors
  • MOO-YEOL Lee, Korea, Republic of
  • Van Q. Do, Korea, Republic of

Abstract

Background and Aims

Smoking is an acknowledged risk factor for vascular disorders, and vascular complication is a main outcome of diabetes. Hence, we investigated the impact of cigarette smoke on blood vessels in diabetes, postulating that smoking might aggravate diabetic vascular impairment.

Methods

Sprague–Dawley rats were divided into four groups: control, cigarette smoke-exposed, diabetic, and cigarette smoke-exposed diabetic groups. Streptozotocin-induced diabetic rats were exposed to cigarette smoke by inhalation at total particulate matter concentration of 200 μg/L for 4 h/day, 5 day/week for a total of 4 weeks.

Results

Diabetes caused structural change of aorta, but additional cigarette smoke exposure did not induce further alteration. Collagen, a marker for fibrosis, was increased in media of diabetic aorta, and this increase was augmented by cigarette smoke. Cigarette smoke induced endothelial nitric oxide synthase (eNOS) uncoupling in the diabetic group. Malondialdehyde was increased and glutathione was decreased in blood from diabetes, but these effects were not exaggerated by cigarette smoke. Cigarette smoke caused NADPH oxidase (NOX) 2 expression in diabetic aorta and enhanced diabetes-induced NOX4 expression in aorta.

Conclusions

Taken together, cigarette smoke exposure can aggravate vascular fibrosis and induce eNOS uncoupling in diabetes under experimental condition, suggesting that smoking might exacerbate diabetic vascular impairments.

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