Assessment of Gelsolin Level in women with heart disease after menopause

 

Wijdan Rajh Hamza Al-Kraity*, Arshad Noori Ghani Al-Dujaili

Biology Department, Faculty of Sciences, University of Kufa, Iraq.

 

ABSTRACT:

In the current study, Seventy menopausal women have CHD were admitted to the coronary care unit of AL-Sader teaching hospital in AL-najaf AL-Ashraf during the period from January to April/2016 for the ages were  ranging  from   40 to 69 years old. The samples were divided into three groups (SA 25, UA 22, AMI 23), while the healthy group was composed of 20. The current study indicated a significant decrease (P<0.05)in serum E2 and GS concentration of CHD compared with healthy group. The serum of E2 and GS concentrations showed a significantly decrease (p<0.05) in AMI compare with UA and SA groups of CHD. The result indicated a positive correlation between E2 and GS. Conclusion: The present study concluded that E2 and GS levels were markers for detection and diagnosis of Coronary heart disease in menopausal women.

 

 

 

 

INTRODUCTION:

Menopause is one of the crucial stages in women’s life which leads to various physiological changes. Menopause is the physiologic cessation of menses associated with the failing ovarian function, maybe diagnosed in retrospect when a year has passed with no menses ¹. Coronary heart diseases (CHD) are the most common cause of morbidity and mortality in most countries ² ,also due to the significant impact of coronary heart disease, it is important for prevention purposes to identify the determinants of risk for developing this disease. coronary artery diseases are the generic designation for the three forms of cardiac diseases, i.e., angina pectoris {unstable angina (UA), stable angina (SA)}, sudden cardiac death and acute myocardial infarction (AMI).

 

Estradiol (E2) is a key sex steroid hormone in females, predominantly synthesized in the ovaries and released into the bloodstream. Estrogen levels decrease dramatically at menopause, which coincides with an increased susceptibility to CVDs³. Gelsolin (GS), by regulating intracellular actin filaments, is important in cell morphology, migration and phagocytosis⁴. Its extracellular isoform, plasma gelsolin is secreted by different types of cells and serves as a scavenging system for potentially toxic actin filaments ⁵. Gelsolin can alter macrophage function by triggering nitric oxide synthase, leading to reduced inflammation ⁶. Previous research has focused on gelsolin’s possible role in cardiovascular diseases; several directions are currently being explored to test whether gelsolin itself can be used as a therapeutic molecule ⁷.

 

MATERIALS AND METHODS:

Patients and healthy groups:

Seventy patients were divided into three study groups: acute myocardial infarction patients group included 23 subjects, unstable angina patients group included 22 subjects and stable angina patients group included 25 subjects, the control group was composed of twenty healthy women. The samples were collected from the coronary care unit (CCU) in Al-Sadder Teaching City in AlNajafprovince/ Iraq, during the period from January till April,2016 .The ages of  patients and control were  ranging from 40 to 69 years old.

 

Collection of blood samples:

Five milliliters of venous blood samples were drown using a disposable needle and plastic syringes from each patients and controls subject. Blood was left at room temperature for 10 minutes to clot, centrifuged 6000 rpm for 10 minutes, and then serum was separated and transported into new disposable tubes.

 

BIOCHEMICAL MEASUREMENT

Determination of serum Estradiol level:

Specific kit for measurement humanestradiol concentrations in serum was supplied by (Accu Bind™., Monobind Inc. USA-Catalog No. 4925-300).

 

Determination of serum Gelsolin level:

Specific kit for measurement human GS concentrations in serum was supplied by Elabscience Biotechnology Co., Ltd. A Catalog No: E-EL-H1786.

 

Statistical Analysis:

The data of present study were articulated as (Mean ± Standard Error), the statistical analysis (descriptive statistics, Correlation coefficients, p value) were calculated by using megastat and Graph pad prism, when P value<0.05 was statistically a significant ⁸.

 

RESULTS:

Comparison of biomarkers between coronary heart disease CHD and healthy group in menopausal women.

The result in figures (1) exhibit significant decrease (p<0.05) in serum levels of E2 and GS (4.338±0.147pg/ml and 179.827±2.663 ng/ml) in CHD group compared with (11.449±0.271pg/ml and 336.740 ± 4.511) in HT group respectively.

 

Figure(1): Comparison of Serum estradiol level between CHD and HT group in menopausal women.

(*) :represent the significant differences at (p<0.05).

 

Figure(2): Comparison of Serum gelsolin level between CHD and HT group in menopausal women.

(*) :represent the significant differences at (p<0.05).

 

Comparison of biomarkers between Stable-angina (SA), Unstable-angina (UA)and Acute myocardial-infarction(AMI) of CHD menopausal women.

The result in figures (3 and 4) exhibit a significant decrease (p<0.05) in serum of E2andGSConcentrations (3.136±0.212pg/ml and 153.894 ±2.067ng/ml) in AMI group and (4.290±0.158pg/ml and 182.364ng/ml ) in UA group compared with (5.589±0.172pg/ml and 203.221±3.050ng/ml) in SA group of CHD respectively.

 

Figure(3): Comparison of Serum estradiol level between SA, UA and  AMI of CHD menopausal women.

The different letters (a, b, c):represent the significant differences (p value < 0.05).

 

Figure(4): Comparison of Serum gelsolin level between SA, UA and  AMI of CHD menopausal women.

The different letters (a, b, c): represent the significant differences (p value < 0.05).

 

The correlation estradiol with gelsolin

The figure(5) indicated, there is  of a significant positive association (P<0.05, r =  0.919) between GS and estradiol concentrations of CHD in menopausal  women.

 

Figure (5): Correlation between serum estradiol and serum gelsolin levels of CHD in menopausal  women.

 

DISCUSSION:

The present study indicate a significant decrease (p>0.05) in serum level estradiol in CHD of menopausal decease in comparison of healthy group. Previous study reported that  following menopause, the decrement in estrogen creation from ovaries due to loss of ovarian functions and depletion of various ovarian hormones caused disturbance of lipoprotein profile, body fat distribution, insulin metabolism, glucose, fibrinolysis, coagulation, vascular endothelium dysfunction ^9-12. Hyperlipidimia and obesity causes atherosclerosis which a key for occurrence angina and myocardial infarction disease, the occurrence of myocardial infarction in women, although lesser than in men, elevates noticeably following menopause, that can be contributed chiefly to the decline of estrogen and its has direct and indirect cardioprotective effects, cardiovascular disease is one of the leading causes of death in women ^13-16 .

 

The current study indicated a significant decrease (p>0.05) in serum gelsolin concentration in CHD groups of menopausal women  in comparison of healthy group. The previous study Lietal.¹⁷ indicated that gelsolin levels had highly a significant difference in the expression between CHD and healthy groups. Another former studies reported that decrement in the concentration of gelsolin in an individual would directly reflect an onset of cellular injury causing either from a trauma, infection or inflammation^18,19. The plasma gelsolin is diminished in the circulation of peoples with ischemic stroke and whether this diminution associates with clinical results in these peoples and  confirmation plasma gelsolin concentration were certainly a significantly diminished in all patients with ischemic stroke compared with healthy peoples and the diminished of plasma gelsolin was conversely correlated to the intensity of systemic inflammation, controlled by an opposite connection with acute phase protein (CRP) concentration ^20,21. The previous studies Suhler et al. ²²and White et al.²³ indicated that the gelsolin levels of platelets poor plasma diminished in SA and UA patients, UA is frequently relation with the rupture of vulnerable atherosclerotic plaques and coronary thrombus formation, The results of these investigations confirmed that actin is expressed into the bloodstream, causing deposition of  F-actin at the elevated concentration of platelet activation of UA patients, and that circulating actin concentrations in excess of Gc-globulin or plasma gelsolin have cytotoxic activities or prothrombotic causing in the strict reduction of plasma elsolin. The Gelsolin releasing was diminished in the medialayer of human atherosclerotic coronary arteries and its expression into the exvivo culture medium was as well diminished^24,25. The reduction of gelsolin may perhaps have problems in vascular functions, in atherosclerosis and coronary heart disease, diminution of gelsolin may well damage ligand interference with macrophage receptors, the modulation on nitric oxide system, and the buffering ability for inflammatory mediators, and other investigations as well support the associations between alterations in gelsolin concentrations and inflammation, oxidative stress, and creation of reactive oxygen species^26,27. The plasma gelsolin sequestration at sites of injury or clearance with circulating actin are the principal causes of diminished plasma gelsolin concentrations after acute damage, the Gelsolin has both antiapoptotic and proapoptotic functions ^28,29.

 

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Accepted on 06.04.2017        © RJPT All right reserved