Salusin-β Levels Research Articles

Evaluation of serum salusin-α and β levels in patients with obstructive sleep apnea.

Aim: Salusin-α and salusin-β peptides are crucial in the development of cardiovascular diseases like coronary artery disease (CAD). This study compared serum levels of these peptides in patients with obstructive sleep apnea (OSA), those with both OSA and CAD.Materials & methods: Patients without OSA were included in Group 1, those with OSA alone comprised Group 2, and those with OSA and CAD were in Group 3.Results: Salusin-α level was significantly higher in controls than in Groups 2 and 3, while salusin-β levels were significantly higher in Groups 2 and 3 compared with the control group.Conclusion: Salusin-α and -β levels may be parameters that can guide the diagnosis of OSA in patients with a consistent clinical history.

Downregulation of salusins alleviates hypertrophic cardiomyopathy via attenuating oxidative stress and autophagy

IntroductionSalusins, which are translated from the alternatively spliced mRNA of torsin family 2 member A (TOR2A), play a vital role in regulation of various cardiovascular diseases. However, it remains unclear precisely regarding their roles in hypertrophic cardiomyopathy (HCM). Therefore, this study was conducted to explore therapeutic effect and the underlying mechanisms of salusins on HCM.Material and methodsIn vivo experiments, Sprague–Dawley rats were used to induce HCM model by angiotensin (Ang) II infusion for 4 weeks. The rats were randomly divided into four groups, namely, Saline + Control shRNA (n = 7), Ang II + Control shRNA (n = 8), Saline + TOR2A shRNA (n = 7), and Ang II + TOR2A shRNA groups (n = 8). After HCM induction, doppler echocardiography is recommended to evaluate heart function. In vitro experiments, primary neonatal rat cardiomyocytes (NRCMs) and cardiac fibroblasts (NRCFs) were obtained from newborn rats, and were treated with Ang II (10–6 M) for 24 h.ResultsAfter treatment with Ang II, levels of salusin-α and salusin-β were elevated in serum and cardiac tissues of rats and in the neonatal rat cardiomyocytes and cardiac fibroblasts. Downregulation of salusins alleviated the Ang II-induced cardiac hypertrophy by suppressing the increased atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and beta-myosin heavy chain (β-MHC) and cardiac fibrosis by blocking collagen I, collagen III and transforming growth factor-beta (TGF-β), and it also attenuated oxidative stress by suppressing the increased reactive oxygen species (ROS) and malondialdehyde (MDA) levels and reversing the decreased superoxide dismutase (SOD) activity and autophagy by inhibiting the increased microtubule-associated protein light chain 3B (LC3B), Beclin1, autophagy related gene (Atg) 3 and Atg5 in the cardiac tissues of Ang II-infused rats and in the Ang II-treated NRCMs.ConclusionsAll these findings suggest that the levels of salusins were elevated in the HCM, and targeting of salusins contributes to alleviation of cardiac hypertrophy and fibrosis probably via attenuating oxidative stress and autophagy. Accordingly, targeting of salusins may be a strategy for HCM therapy.

The relationship of salusins with Parkinson's Disease, Alzheimer's Disease, and acute ischemic stroke: A preliminary study

Neuroinflammation, oxidative stress, and apoptosis play important roles in the pathophysiology of Alzheimer’s Disease (AD), Parkinson’s Disease (PD), and Acute Ischemic Stroke (AIS). Salusin-α and salusin-β peptides, which were shown to be present in many tissues, including the central nervous system, were also shown to be associated with apoptosis, inflammation, and oxidative stress. In the present study, the relationship between Salusin-α and salusin-β peptides and AD, PD, and AIS were investigated.A total of 179 people were included in the present study, including 46 AD, 44 PD, 42 AIS, and 47 controls. Plasma Salusin-α and salusin-β levels were measured with the ELISA Method.The plasma salusin-β levels of AD, PD, and AIS patients were lower than the control group at significant levels (p < 0.05). It was also found that there were correlations between salusin-α and salusin-β levels and age, triglyceride, LDL-c, total cholesterol, and hemoglobin levels.In this study, we found that salusin- β, an endogenous neuropeptide, was associated with AD, PD and AIS. The low level of salusin-β in these diseases in which neuronal damage occurs may be related to the neuroprotective properties of this endogenous peptide. Further studies are needed to fully understand the relationship between salusin-β and the pathophysiology of these diseases.

Serum salusin-α and -β levels in patients with parkinson's disease.

The etiology of Parkinson's disease (PD) is not well known and there is increasing evidence that oxidative stress also plays an important role in its pathogenesis. Salusins alpha (salusin-α) and beta (salusin-β) affect the central nervous system, vasculature, and kidneys to increase the inflammatory response in endothelial cells, stimulate oxidative stress, and increase monocyte-endothelial adhesion. Neuroinflammation and oxidative stress play roles in the etiopathogenesis of PD. To investigate whether salusin-α and -β are related to PD and whether they are correlated with the development of atherosclerosis, body mass index, disease duration, and the Parkinson's Hoehn and Yahr stage. The low-density lipoprotein cholesterol (LDL-C), total cholesterol, and salusin-β levels were significantly lower and age was significantly higher in Parkinson patients compared to healthy controls (ρ < 0.005). We found a negative linear correlation between salusin-β and the Hoehn and Yahr stage (ρ < 0.001, r = -0.515) in the patients. There was a relationship between salusin-β and PD and a correlation between the salusin-β levels and Parkinson's stage. A possible underlying disease mechanism is an increase in oxidative stress and decrease in neuroprotective effects due to low salusin-β levels. Therefore, the effects of salusin-β in treating Parkinson disease should be evaluated. Further studies are needed to understand the effects of salusin-β treatment on preventing or slowing the course of PD.

Comparison of the effect of resistance versus aerobic exercise on the serum levels of salusin-α and salusin-β, lipid profile and insulin resistance in overweight/obese women

Comparison of the effect of resistance versus aerobic exercise on the serum levels of salusin-α and salusin-β, lipid profile and insulin resistance in overweight/obese women

Serum salusin-β levels in patients with systemic lupus erythematosus.

Endothelial dysfunction (ED) has an important role in the pathogenesis of systemic lupus erythematosus (SLE). Studies on other inflammatory diseases show that salusin-β with various mechanisms may play a role in the promotion of ED and inflammation. The aim of this study was to measure serum salusin-β levels in SLE patients and evaluate it as a potential biomarker in assessing SLE activity and predicting organ involvement. In a cross-sectional study, 60 patients diagnosed with SLE and 30 age- and sex-matched healthy controls were enrolled. Disease activity of SLE patients was assessed by the systemic lupus erythematosus disease activity index 2000 (SLEDAI-2K). Serum levels of salusin-ß were measured using a human salusin-ß enzyme-linked immunosorbent assay kit. Serum salusin-β levels in SLE and control groups were 474.2 ± 117.1pg/ml and 157.7 ± 88.7pg/ml, respectively. The difference was significant (P = 0.001). There was no significant correlation between serum salusin-β levels with age (r = - 0.06, P = 0.632) and SLEDAI (r = - 0.185, P = 0.158). In patients with nephritis and thrombosis, serum salusin-β was significantly higher. In addition, in patients with serositis, serum salusin-β was significantly lower. Multiple linear regression analysis showed that serum salusin-β levels retained a significant association with nephritis and thrombosis after model adjustment for serositis, nephritis, and thrombosis. Our findings showed that salusin-β might have a possible role in the pathogenesis of SLE. Salusin-β may be a potential biomarker for nephritis and thrombosis in SLE. Key Points • Serum salusin-β levels were significantly higher in SLE patients than the control group. • There was no significant correlation between serum salusin-β levels with age and SLEDAI. • Serum salusin-β levels retained a significant association with nephritis and thrombosis.

Serum salusin-α and salusin-β levels in patients with psoriatic arthritis

Psoriatic arthritis (PsA) is a chronic inflammatory disease characterized by skin lesions and joint involvement. Salusin-α and salusin-β are two new bioactive molecules. It is reported that salusins may have role in regulation of the immune system and inflammation. The aim of our study was to evaluate the serum salusin-α and salusin-β levels in PsA patients and to establish the possible relationship with the disease features. Our study included 40 PsA patients who fulfilled the CASPAR criteria and 40 healthy volunteers. Demographic, clinical, laboratory and radiological data and disease activity indices (PASI, BASDAI, BASFI, HAQ) were recorded in all patients. The enzyme-linked immunosorbent assay (ELISA) method was used to measure serum salusin-α and salusin-β levels. The demographic data were as follows: 13 patients (32.5%) were males and 27 (67.5%) were female, mean age was 48.5 years and mean disease duration was 2.4 years. Patients' history was taken and clinical assessment was performed; 20 (50%) patients had a family history, 18 (45%) patients were smoker, 19 (47.5%) patients had HLA-B27 positivity, 33 (82.5%) had sacroiliitis, 36 (90%) had enthesitis, 23 (57.5%) had distal interphalangeal (DIP) joint and nail involvement, 26 (65%) had wrist involvement, and 11 (27.5%) had ankle involvement. Laboratory data of the patients were recorded; 20 (50%) patients had elevated CRP level and 25 (62.5%) patients had an elevated ESR level. The study results showed that PsA patients had an elevated serum salusin-α level when compared with the control group (p = 0.004). The association between serum salusin-α level and ankle arthritis was found (p = 0.04). Serum levels of salusin-β were similar in PsA patients and controls both (p = 0.285). We found elevated serum salusin-α in PsA patients while the serum salusin-β levels were normal. Salusin-α may have a possible role in disease pathogenesis and it may be use as a reliable biomarker in PsA patients. Multicenter prospective studies are needed in this regard.

A New Insight Into Pathophysiological Mechanism of Abdominal Aortic Aneurysm With Novel Parameters Salusin-β and Arterial Stiffness

Abdominal aortic aneurysm (AAA) has risk factors similar to those of atherosclerosis. Salusin-β and arterial stiffness are novel parameters that have been shown to predict atherosclerosis and related cardiovascular disorders. However, their predictive value for detecting AAA remains unclear. Forty-eight patients with AAA and 47 age- and sex-matched participants without AAA were enrolled in the study. Arterial stiffness parameters were obtained via an oscillometric Mobil-O-Graph PWA Monitor device (IEM GmbH) with integrated ARCSolver software (Australian Institute of Technology). Plasma salusin-β levels were analyzed using an enzyme-linked immunosorbent assay reagent kit (Abbkine, Inc). The measured salusin-β levels and arterial stiffness parameters of the AAA and control groups were compared. Salusin-β levels were significantly lower in patients with AAA (P = .014). There was a significant negative correlation between salusin-β levels and abdominal aorta diameter. No significant difference was detected between AAA and control groups in terms of arterial stiffness parameters (P > .05). In backward multiple regression analysis, the presence of AAA, platelet count, and augmentation index were found to be independent predictors of salusin-β levels (P = .006 and P = .023, respectively). Arterial stiffness parameters were not found to be associated with AAA. Contrary to previous results regarding atherosclerosis and related cardiovascular disorders, salusin-β levels were found to be lower in patients with AAA. Although AAA is thought to have similar risk factors as atherosclerosis, the exact pathophysiologic mechanism remains unclear.

Saluisn-β contributes to endothelial dysfunction in monocrotaline-induced pulmonary arterial hypertensive rats

BackgroundThe endothelial dysfunction and the consequent attenuated pulmonary vasodilatation are the major causes of elevated pulmonary arterial resistance and pressure in pulmonary arterial hypertension (PAH). Current study aimed to explore the effects of a TOR2A gene product, salusin-β, on endothelium-dependent vascular relaxation and the progression of PAH in monocrotaline (MCT)-induced PAH rats as well as the relevant signaling pathway. MethodsAcetylcholine (ACh)-induced dose-dependent relaxation was used to evaluate the endothelium-dependent vasodilatation function. ResultsThe salusin-β level in plasma and pulmonary artery (PA) in MCT-PAH rats were significantly increased, while the ACh-induced endothelium-dependent vasodilatation was attenuated. After salusin-β incubation or overexpression of salusin-β gene, the endothelium-dependent relaxation was further deteriorated, while anti-salusin-β IgG incubation or knockdown of salusin-β improved it in PAH rats. The superoxide anions scavenger NAC or the antioxidant apocynin inhibited the effect of salusin-β, while the SOD inhibitor DETC further enhanced it. The nitric oxide (NO) synthase inhibitor L-NAME almost blocked the effect of anti-salusin-β IgG. Silencing of salusin-β in PAH rats decreased right ventricular (RV) systolic pressure, RV hypertrophy index, NAD(P)H oxidase activity and ROS level, and increased the eNOS activity and NO level of PA. Overexpression of salusin-β played opposite roles. ConclusionsThe elevated saluisn-β level in PAH rats plays important roles in the reduction of endothelium-dependent vasodilatation and participates in the progression of PAH through stimulating NAD(P)H oxidase-ROS production and inhibiting eNOS-NO release.

Association Between Dermcidin, Salusin-α, Salusin-β Molecules and Diabetic Foot Infections.

Dermcidin, salusin-α, and salusin-β are three recently discovered molecules that confer antimicrobial properties. The present study aims to investigate the association between dermcidin, salusin-α, and salusin-β in the etiopathology of patients with diabetic foot infection. The study included three groups: Group 1 - diabetic foot infection; Group 2 - diabetes without history of diabetic foot; and Group 3 - the control group. Plasma dermcidin, salusin-α, and salusin-β levels were compared across the groups. Median (Q1-Q3) values of plasma dermcidin levels in Groups 1, 2, and 3 were 3.45 (0.8-4.4), 5.2 (3.7-6.4), and 5.8 (3.1-10) ng/mL, respectively. Diabetic foot infection group had significantly lower plasma dermcidin levels compared to diabetes only group and control group (P = .000, ANOVA), whereas there was no statistically significant difference between the Group 2 and Group 3 (P = .163, ANOVA). Salusin-α and salusin-β levels were significantly higher in the Group 3 compared to the other groups. Based on our findings, diabetic foot infection group had significantly lower plasma dermcidin levels and salusin-α and salusin-β levels were significantly higher in the control group. These molecules (dermcidin specifically) can be researched as an adjuvant therapeutic agent in addition to conventional treatments in diabetic foot diabetic foot infections. Also, it can be searched this may prevent many complications including amputation.

Salusin-β in patients with subclinical hypothyroidism and low to moderate cardiovascular disease risk

Abstract :BACKGROUND AND OBJECTIVES: Because Subclinical hypothyroidism may be a risk factor for cardiovascular disease, we aimed to measure the level of salusin-β which is a new biomarker for predicting atherosclerotic cardiovascular diseases (CVD) in those patients.PATIENTS AND METHODS: 57 subclinical hypothyroid patients were compared with a control group of 60 euthyroid subjects whose age and sex were matched to the patient group. Both groups have low to moderate 10-year risk of fatal CVD. We studied the serum level of salusin-β in the selected group of SC hypothyroid patients to find out if it can be used as an indicator of the cardiovascular adverse effects in them. We also studied the association between salusin-β levels and TSH level, thyroid Ab, and individual’s risk of CVD.RESULTS: Salusin-β was higher in the SC hypothyroidism group with a significant difference (p = 0.001). TSH, FT4, diastolic BP and triglycerides showed a significant difference between the two groups. Systolic BP, total cholesterol, smoking, and SCORE showed no significant difference between the two groups. There was a highly +ve correlation with TSH level in the SC hypothyroid group.Conclusion:The elevated salusin-𝛽 level supports the opinion that SC hypothyroidism has a cardiovascular risk and can support treatment of these cases whose TSH < 10 mIU/l.KEYWORDS: salusin-β, Subclinical hypothyroidism, cardiovascular disease risk.

Evaluation of salusin-α and salusin-β levels in patients with type 2 diabetes mellitus and determination of the impact of severity of hyperglycemia on salusin levels.

To investigate the usefulness of salusin-α and salusin-β as biomarkers in patients with type 2 diabetes mellitus (T2DM) and to determine whether diabetes severity and obesity have an effect on the salusin levels in diabetic patients. The study included a total of 90 patients, comprising 55 diagnosed with T2DM and 35 healthy volunteers with similar demographic characteristics. Salusins were assayed by a commercially available ELISA kit. The salusin-β levels were found to be significantly higher in T2DM group compared to control group, while the salusin-α levels were lower (p < 0.05, for both). Furthermore, in patient group, Spearman analysis showed a statistically significant negative correlation between salusin-α and fasting glucose and glycated hemoglobin (HbA1c), whereas salusin-β had a statistically significant positive correlation with fasting glucose and HbA1c (p < 0.05, for both). When analyzed according to the HbA1c groups, the patients with HbA1c > 9% had significantly lower salusin-α and higher salusin-β levels levels compared to those with HbA1c < 9% (p < 0.05, for both). When examined according to body-mass-index groups, there was no significant difference in the salusin levels of the patient and control groups (p > 0.05). We demonstrated that the serum salusin-α level was decreased whereas the salusin-β level was increased in patients with T2DM compared to healthy subjects, and this was more pronounced as T2DM-deteriorated. We also showed that obesity had no effect on salusin levels among diabetics. This study may provide a basis for the availability of salusin-targeted therapies, especially in uncontrolled T2DM.

Salusin-β Mediates High Glucose-Induced Inflammation and Apoptosis in Retinal Capillary Endothelial Cells via a ROS-Dependent Pathway in Diabetic Retinopathy

BackgroundDiabetic retinopathy (DR) is characterized by retinal vascular endothelial cell death and vascular inflammation, which are microvascular complications of diabetes mellitus (DM). Salusin-β, a newly identified peptide, is closely associated with hypertension, atherosclerosis and diabetic cardiomyopathy. However, the exact role of salusin-β in high glucose (HG)-induced retinal capillary endothelial cell (REC) inflammation and apoptosis remains unclear.Patients and MethodsA total of 60 patients with type 2 diabetes and 20 healthy controls were included in this study. Based on fundus fluorescein angiography findings, the diabetic patients were divided into three subgroups: diabetes without retinopathy (DWR), non-proliferative DR (NPDR) and proliferative DR (PDR). Serum salusin-β levels were measured by enzyme-linked immunosorbent assay. Human RECs (HRECs) were cultured in normal glucose (NG) and HG medium with or without salusin-β. Salusin-β expression was analysed by Western blotting and immunofluorescence staining. Expression of the pro-inflammatory cytokines MCP-1, IL-1β, TNF-α, and VCAM-1 was analysed by Western blotting. Reactive oxygen species (ROS) production was measured with 2′,7′-dichlorofluorescein diacetate (DCFH-DA). Cell apoptosis rates were determined by flow cytometry. The levels of p38, JNK, p-p38, and p-JNK and the apoptosis-related proteins cleaved caspase-3, Bax, and cl2 were analysed by Western blotting.ResultsSerum salusin-β levels were higher in diabetic patients than in healthy controls (p = 0.0027), especially in patients with NPDR and PDR (both p<0.01). HG upregulated salusin-β expression in HRECs in a time-dependent manner. Salusin-β exacerbated inflammation and apoptosis, upregulated intracellular ROS production in HG-induced HRECs, and activated ROS-dependent JNK and p38 MAPK signalling, while knockdown of salusin-β suppressed these effects.ConclusionOur findings indicate that salusin-β can promote inflammation and apoptosis via ROS-dependent JNK and p38 MAPK signalling in HG-induced HRECs and could be a therapeutic target for DR.

The role of serum salusin alpha and beta levels and atherosclerotic risk factors in idiopathic sudden hearing loss pathogenesis.

The aim of this study was to investigate the importance of atherosclerosis in the pathogenesis of sudden hearing loss by evaluating the newly discovered markers, serum salusin-α and salusin-β. We also aimed to evaluate atherosclerosis risk factors, such as lipid profile, smoking, body mass index, waist circumference and mean blood pressure of the patients. Fifty-two patients diagnosed with sudden hearing loss (study group) and fifty healthy people (control group) were included in the study. Detailed history was taken from the patients and risk factors for atherosclerosis, such as smoking, body mass index, waist circumference, lipid profile, mean blood pressure and serum salusin-α and salusin-β levels, were evaluated. The study group was divided into recovery group (subgroup I) and non-recovery group (subgroup II). The salusin-β median value was found to be significantly higher in the study group compared to the control group (p < 0.05). The salusin-β median value was found to be significantly higher in subgroup 2 and was found to be a poor prognostic factor (p < 0.05). From the results obtained in this study, it is thought that salusin-β peptide is increased in patients with sudden hearing loss and it can be evaluated as a poor prognostic factor.

Improvement of Vascular Function by Knockdown of Salusin-β in Hypertensive Rats via Nitric Oxide and Reactive Oxygen Species Signaling Pathway.

PurposeSalusin-β, a multifunctional vasoactive peptide, has a potentially important function in the pathological development of hypertension. However, the exact functional role of salusin-β and the underlying mechanism in this process are still not fully understood. The current study aimed to investigate the effects of silencing salusin-β on vascular function and vascular remodeling, as well as its signaling pathways in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY).MethodsSilencing salusin-β was performed by caudal vein injection of adenovirus expressing salusin-β short hairpin RNA (shRNA). Acetylcholine (ACh)-induced endothelium-dependent relaxation was used to evaluate vasodilator function, and high K+ solution-induced constriction was used to evaluate vasoconstriction function.ResultsSalusin-β levels in plasma and its protein expression in mesenteric artery (MA), coronary artery (CA), and pulmonary artery (PA) of SHR were higher than those in WKY. The salusin-β level and expression were decreased effectively by salusin-β shRNA. Knockdown of salusin-β decreased arterial blood pressure (ABP) and high K+ solution-induced vascular constrictions, and improved the endothelium-dependent relaxation and vascular remodeling in SHR. The improved effect of silencing salusin-β on ACh-induced relaxation in SHR was almost blocked by the nitric oxide synthase (NOS) inhibitor L-NAME. Compared to WKY, the endothelial NOS (eNOS) activity and level, and nitric oxide (NO) level were decreased, while NAD(P)H oxidase activity and reactive oxygen species (ROS) levels in MA, CA, and PA of SHR were increased, which were all redressed by salusin-β knockdown.ConclusionThese results indicate that knockdown of salusin-β improves endothelium-dependent vascular relaxation and vascular remodeling and decreases ABP and vasoconstriction in SHR, which might be accomplished by increasing eNOS activation and NO release while inhibiting NAD(P)H oxidase derived-ROS generation. Scavenging salusin-β improves vascular function and then prevents the development and progression of vasculopathy of hypertension.

Downregulation of Salusin-β protects renal tubular epithelial cells against high glucose-induced inflammation, oxidative stress, apoptosis and lipid accumulation via suppressing miR-155-5p

ABSTRACT Diabetic nephropathy (DN) is the main contributor to the excess mortality for patients suffering from diabetes. Here, C57BL/6 mice received 4 weeks of high-fat diet and intraperitoneal injection of STZ (100 mg/kg). Mice with random blood glucose level ≥16.7 mmol/L and positive urine protein were recognized as successful DN model. To construct an in vitro model, HK-2 cells were incubated with 30 mM glucose. RT-qPCR and western blot were employed to measure Salusin-β levels in kidney tissues of DN mice and HG-induced HK-2 cells. Meanwhile, RT-qPCR was performed to detect miR-155-5p level in kidney tissues of DN mice and HG-induced HK-2 cells. TNF-α, IL-6, IL-1β, ROS, SOD and CAT levels were assessed using commercial assay kits. Furthermore, apoptosis of HK-2 cells was assessed via flow cytometric analysis and TUNEL staining. In addition, intracellular lipid accumulation and total cholesterol levels were detected using Oil red O staining and TC ELISA kit. Herein, Salusin-β and miR-155-5p levels were distinctly upregulated in kidney tissues of DN mice and HG-induced HK-2 cells. Downregulation of Salusin-β reduced miR-155-5p expression. Salusin-β silencing dramatically relieved inflammatory and oxidative injury, suppressed apoptosis as well as lipid accumulation induced by HG in HK-2 cells. Besides, miR-155-5p elevation partially abrogated the alleviating effects Salusin-β silencing on HG-induced RTEC injury. In summary, downregulation of Salusin-β protected HK-2 cells against HG-induced inflammation, oxidative stress, apoptosis and ameliorated lipid accumulation through suppressing miR-155-5p, which indicated that Salusin-β could be a potential therapeutic drug for DN.

Novel risk factor for fatal arrhythmia in Brugada syndrome

Abstract Background Brugada syndrome (BrS) is a genetic disease associated with increased risk of ventricular fibrillation (VF)/ventricular tachycardia (VT). The VF/VT in BrS occurs more frequently during a night time or at a rest with parasympathetic nerve activation. Some risk factors of VF/VT occurrence in BrS have been elucidated, however, it remains controversial about risk stratification. Salusin-β is an endogenous bioactive peptide that systemically exerts rapid and profound hypotensive and bradycardic activities and parasympathomimetic hemodynamic actions in vivo. Previous reports suggested that salusin-β is suppressed following physiological parasympathetic stimulation and appears to constitute a negative feedback relationship with the parasympathetic nervous system. Purpose We hypothesized that salusin-β is associated with the occurrence of VF/VT in BrS. Methods The study population consisted of 26 BrS patients with newly implantation of implantable cardioverter defibrillator (ICD) during 2003–2008. In all patients, salusin-β was measured in supine position after 20 minute rest. The date of salusin-β sampling was set as the registration point for this study. The VF/VT was defined as any episode of fatal ventricular tachyarrhythmia or any appropriate shock. In accordance with the presence or absence of VF/VT events within 5 years, all patients were divided into VF/VT group (n=6) and non-VF/VT group (n=20).Various clinical parameters were compared between the two groups. For analysis of autonomic nervous function, heart rate variability (HRV) and pupil function were evaluated. Results The mean age was 54±17 years old. There is no differences between the two groups in clinical parameters. In analysis of HRV, the high-frequency component (0.15–0.40 Hz; HF), low frequency component (0.04–0.15 Hz; LF) and the LF/HF ratio were analyzed over 24 h. LF/HF ratio was significantly lower over 24h in VF/VT groups in comparison with non-VF/VT groups [day-time; 1.8 (1.2–5.6) vs. 5.2 (3.4–8.8), p=0.048, night-time; 1.2 (1.1–1.3) vs. 3.9 (2.5–8.7), p=0.003]. Furthermore, in analysis of pupil function, right/left miosis ratio was higher in VT/VF groups in comparison with non-VT/VF groups [right pupil; 0.39 (0.37–0.59) vs. 0.34 (0.28–0.38), p=0.035, left pupil; 0.43 (0.36–0.50) vs. 0.33 (0.28–0.40), p=0.049]. In plasma total salusin-β levels, the VF/VT groups exhibited significantly lower than non-VF/VT groups (55.2±14.6 vs. 73.2±22.2, p=0.039, Figure). Conclusions Salusin-β was associated with the occurrence of VF/VT in Brugada syndrome. Salusin-β might be useful to identify high-risk patients for the occurrence of VT/VF events in Brugada syndrome. Funding Acknowledgement Type of funding source: None

Serum salusin-β in relation to atherosclerosis and ventricular dysfunction in patients with type 2 diabetes mellitus

Background and aimsSalusin-β is a newly defined biomarker that plays a role in atherogenesis and in homeostasis. The study aimed to assess serum salusin-β level in relation to atherosclerosis and ventricular dysfunction in type 2 diabetes mellitus (T2DM) patients. MethodsSixty T2DM patients and twenty-five age-matched healthy controls were included. Serum salusin-β was determined by ELISA. Echocardiography and carotid ultrasonography were carried out for all individuals. ResultsSerum salusin-β level was significantly elevated in patients with T2DM than in controls (P < 0.001). It was positively correlated with obesity parameters, insulin resistance index (r = 0.280,P < 0.001), atherogenic dyslipidemia and with carotid intima media thickness (CIMT) (r = 0.411, P < 0.001). Echocardiographic findings showed a positive correlation between salusin-β and left ventricular hypertrophy (LVH) parameters and a negative correlation with left ventricular (LV) diastolic and systolic functions. Regression analysis showed that serum salusin-β level was a significant predictor of diastolic dysfunction. ConclusionSerum salusin-β may be associated with atherosclerosis and LV dysfunction in T2DM.

The importance of circulating levels of salusin-α, salusin-β, and heregulin-β1 in atherosclerotic coronary arterial disease

ObjectiveThe relationship between the severity of atherosclerotic coronary artery disease (CAD) and circulating levels of salusin-α, salusin-β and heregulin-β1 has been investigated. In addition, the relationship with these peptides and high sensitive C-reactive protein (hsCRP) has been investigated. MethodsThe study was conducted on 55 volunteers who had normal coronary angiography (CAG) as the control group, 35 volunteers with the degree of coronary artery stenosis below 50% in CA as the non-critical stenosis group, 37 volunteers with narrowing of one coronary artery above 50% as single vessel group and 41 volunteers with narrowing of more than one coronary artery above 50% as multi-vessel group. One hundred and thirteen volunteers have been included to CAD group. ResultsThere was no statistically significant difference in serum salusin-α levels between groups. Serum salusin-β ve hsCRP levels were significantly lower in control group compared to other groups and CAD group. There was no statistically significant difference in salusin-β and salusin-α levels in reciprocal comparison of other groups other than heregulin-β1 levels. Heregulin-β1 levels were significantly lower in 'non-critical occlusion' and 'multiple artery occlusion' groups compared to control group. Heregulin-β1 levels in 'single artery occlusion' group were significantly higher than control, 'non-critical occlusion' and 'multiple artery occlusion' groups. ConclusionSalusin-α levels does not indicate any significant differences between any groups in our study however the relationship of salusin-α with salusin- β and heregulin-β1 levels drives to cogitate that these peptides can be used as biomarkers and therapeutic approaches in CAD. We think that these peptides will be used in laboratories routinely in future in addition to hsCRP for CAD.

Evaluation of Serum Level of Salusin Beta in Psoriatic Patients

Psoriasis is a chronic, immune-mediated, inflammatory disease of the skin. It is a multifactorial malady with hereditary foundation activated by enviromental factors and immunological middle people. Numerous Epidemiologic examinations proposed that patients with psoriasis are at expanded danger of cardiovascular disease.To assess serum salusin beta level in psoriatic patients. In this relative case-control study, 50 psoriatic patients (case gathering) and 30 age-and sexual orientation coordinated solid people filling in as a benchmark group, were chosen from the outpatients' facilities of the Dermatology, Venereology, and Andrology Department, Faculty of Medicine, Benha University, during the period from October, 2018 to May, 2019. This investigation found that the serum salusin-β levels were signifcantly higher in psoriasis patients contrasted with control group.This study found that the serum salusin-β levels were signifcantly higher in psoriasis patients contrasted with control gathering.