Protective effect of cinnamon extract against cobalt-induced multiple organ damage in rats.

Background: The role of oxidative stress and inflammation in cobalt (Co) toxicity has been the focus of previous studies. Cinnamon and its main components have been reported to have protective effects in various tissues with antioxidant and anti-inflammatory effects. Aims: In this study, the protective effect of cinnamon extract (CE) against possible Co-induced heart, kidney, and liver damage in rats was investigated biochemically. Methods: Eighteen albino Wistar-type male rats were categorized into three groups (n = 6 per group): control (CG), CoCL2-administered (CoCL2), and CE + CoCL2-administered (CE + Co) groups. The CE + CoCL2 group was administered CE (100 mg/kg), and the CoCL2 and CG groups were administered distilled water orally by gavage. One hour after the administration, Co (150 mg/kg) was administered orally to the CE + CoCL2 and CoCL2 groups. This procedure was repeated once daily for 7 days. Then, biochemical markers were studied in the excised heart, kidney, and liver tissues. Results: CoCL2 increased oxidants and proinflammatory cytokines and decreased antioxidants in heart, kidney, and liver tissues. Heart, kidney, and liver tissue were affected by Co damage. CE treatment suppressed the CoCL2-induced increase in oxidants and proinflammatory cytokines and decrease in antioxidants in heart, kidney, and liver tissues. CE treatment has been shown to attenuate cardiac damage by reducing serum troponin I (TpI) and creatine kinase-MB (CK-MB), renal damage by reducing creatinine and blood urea nitrogen (BUN), and liver damage by reducing alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Conclusion: Co induced the production of oxidants and proinflammatory parameters and antioxidant depletion in heart, kidney, and liver tissues of rats. Our experimental results show that CE protects heart, kidney, and liver tissues against oxidative and inflammatory changes induced by CoCLl2.

Serum salusin-α levels in systemic lupus erythematosus and systemic sclerosis.

OBJECTIVE: Systemic lupus erythematosus (SLE) and systemic sclerosis (SSc), chronic inflammatory diseases, demonstrate an increased incidence of cardiovascular manifestations and subclinical atherosclerotic disease. Salusin-α is a novel bioactive peptide that suppresses the formation of macrophage foam cells, and its serum level is significantly lower in patients with angiographically proven coronary artery disease. The aims of the study were to assess serum salusin-α level and its potential association with the predictors of atherosclerosis in SLE and SSc. MATERIAL AND METHODS: The study included 20 SLE and 22 SSc patients and 23 healthy controls (HC). All of the participants were female. Tumour necrosis factor-α (TNF-α), IL-6 and salusin-α levels, homeostasis model assessment for insulin resistance (HOMA-IR) index and common carotid intima-media thickness (IMT) were determined. RESULTS: Salusin-α levels were lower and the IMTs were higher in the SLE and SSc groups than in the HC group. The salusin-α level was correlated with neither the disease activity scores nor cytokine levels and IMT in the SLE and SSc groups, although it was correlated with triglyceride level in the SLE group (r=-0.564, p=0.012), and with HOMA-IR index in the HC group (r=0.485, p=0.019). CONCLUSION: The present preliminary study may support the idea that SSc leads to subclinical atherosclerosis, as in SLE. Moreover, it can be concluded that the decreased salusin-α levels in SLE and SSc may contribute to subclinical atherosclerosis. However, further studies with larger sample size are needed to demonstrate this contribution in SLE and SSc.

Prevalence and significance of MEFV gene mutations in a cohort of patients with rheumatoid arthritis.

OBJECTIVES: Pyrin/marenostrin, an inhibitory regulator of inflammation, is encoded by MEditerranean FeVer (MEFV) gene. Mutations of this gene are the cause of familial Mediterranean fever (FMF). A connection between MEFV gene mutations and rheumatic diseases has been suggested. The aim of this study was to explore the frequency and clinical significance of MEFV gene mutations in a cohort of Turkish patients with rheumatoid arthritis (RA). METHODS: The study included 103 patients with RA and 103 age-, sex- and origin-matched healthy controls (HC). In all participants, genomic DNA was isolated and genotyped using amplification refractory mutation system or restriction fragment length polymorphism for the eight MEFV gene mutations (E148Q, M694V, M694I, M680I, V726A, A744S, R761H, and P369S). In the RA group, disease activity was determined using the disease activity score-28 (DAS-28), and radiological damage was evaluated by the modified Larsen scoring method. RESULTS: Carrier rates of MEFV gene mutations were 26/103 (25.2%) and 24/103 (23.3%) in the RA and HC groups, respectively (p>0.05, OR: 0.9, 95% CI: 0.48-1.71). In the RA group, while deformed joint count was significantly higher in the mutation carrier group than those of the non-carrier group (p<0.05), the level of C-reactive protein, DAS-28 and modified-Larsen scores were slightly but not significantly higher in the carrier group. CONCLUSION: The results of this study suggest that MEFV gene mutations appear to be an aggravating factor for the severity of RA, and consequently, patients with RA might be screened for MEFV gene mutations in countries where FMF is frequent. Whether the searching of MEFV gene mutations in RA patients is cost-effective deserves further investigations.