Abstract

BackgroundEpidemiological studies reported that diabetic patients had a lower incidence of aortic dissection (AD), but the definite mechanism is unknown. We aim to investigate the possible protective effect of diabetes mellitus (DM) on AD formation with an emphasis on autonomic remodeling.MethodsStreptozotocin (STZ) intraperitoneal injection was applied to induce diabetes, unilateral renal artery stenosis (URAS) together with β-amino propionitrile (BAPN) oral treatment was used to induce AD. Sixty SD rats were equally and randomly divided into four groups (normal group, DM group, URAS + BAPN oral treatment group, DM + URAS + BAPN oral treatment group). Rats were fed for 6 weeks, the number of AD was recorded and remained rats were sacrificed. Thoracic aorta were harvested, morphological changes were assessed. Expression of tyrosine hydroxylase (TH), choline acetylase (ChAT), matrix metalloprotease 2 (MMP2) and matrix metalloprotease 9 (MMP9) were evaluated.ResultsA total of 7 AD was noted in S + B group, DM rats did not develop AD. Diabetic rats had a lower incidence of AD (P < 0.01). In dissected aorta, collagen deposition increased while elastic fiber became fragmented. These pathological changes diminished in diabetic rats. Diabetic rats had a lower expression of ChAT (P < 0.01). URAS + BAPN treatment elevated expression of TH in normal rat and ChAT in diabetic rats (P < 0.001). Expression of MMP2 and MMP9 elevated in all the rats after URAS + BAPN, but the elevation range of MMP2 in diabetic rats was smaller (P < 0.001).ConclusionsSTZ-induced diabetic rats have a lower incidence of AD after URAS and BAPN treatment, this protective effect could be possibly attributed to autonomic innervation modification and possible related down-regulation of MMP2.

Highlights

  • Epidemiological studies reported that diabetic patients had a lower incidence of aortic dissection (AD), but the definite mechanism is unknown

  • Sympathetic hyperactivity was detected in patients with thoracic aortic dissection (TAD) [7], further investigation revealed that noradrenaline (NE) release from sympathetic nerve endings would upregulate matrix metalloprotease 2 (MMP2) expression in thoracic aorta which may lead to Extracellular matrix (ECM) reconstruction [8], these results showed a direct correlation between autonomic nervous system (ANS) and AD

  • We aim to investigate the negative association between diabetes mellitus (DM) and AD with an emphasis on autonomic remodeling of aorta via an animal model of superimposed diabetes on aortic dissection

Read more

Summary

Introduction

Epidemiological studies reported that diabetic patients had a lower incidence of aortic dissection (AD), but the definite mechanism is unknown. Hu et al BMC Cardiovascular Disorders (2016) 16:200 been found to be a crucial modulator of ECM remodeling in thoracic aorta for a long time. Fronek [5] noticed a dramatic increase of collagen content and histological changes of elastin in thoracic aorta after chemical sympathectomy. Angouras [6] demonstrated that the density of collagen and elastin in thoracic aorta increased significantly after bilateral surgical sympathectomy. The relationship between ANS and ECM remodeling in aortic disease has been seldom studied before. Sympathetic hyperactivity was detected in patients with TAD [7], further investigation revealed that noradrenaline (NE) release from sympathetic nerve endings would upregulate matrix metalloprotease 2 (MMP2) expression in thoracic aorta which may lead to ECM reconstruction [8], these results showed a direct correlation between ANS and AD

Objectives
Methods
Results
Discussion
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.