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Hamid Yaghooti, Mohsen Firoozrai and Mohammad Reza Khorramizadeh

Abstract

Background: Cadmium (Cd) is an extremely toxic metal commonly found in industrial work places, a food contaminant and a major component of cigarette smoke. Tobacco smoke and Cd inhalation result in alveolar inflammation, accumulation of immune cells and proteases/anti-proteases imbalance associated with chronic obstructive pulmonary disease and emphysema.

Objectives: We studied Cd toxicity on U-937 monocytoid cells and its influence on matrix metalloproteinase-9 (MMP-9) and its tissue inhibitor (TIMP1) levels.

Methods: U-937 cells were cultured and treated with either concentrations of 1.0, 10.0 or 50.0 μM cadmium chloride. Cytotoxicity percentages were measured by activity assay of lactate dehydrogenase released into culture medium of treated and the control cells. MMP-9 and TIMP-1 levels were determined by ELISA. Zymography technique was used to quantify MMP-9 gelatinolytic activity in culture media of U-937 cells. Alterations in MMP-9 and TIMP-1 gene expressions in response to Cd were analyzed by real-time PCR method.

Results: Cd found to be dose-dependently cytotoxic where 50.0 μM Cd significantly increased LDH leakage from the cells (p <0.05). MMP-9 levels measured by ELISA and zymography methods showed significant 44% and 48% increase, respectively, following exposure to 50.0 μM of Cd (p <0.05). Cd doses did not exert any effect on TIMP-1 levels. Alteration in MMP-9/TIMP-1 genes expressions in response to Cd found to be below a half fold increase for all doses which were not statistically significant.

Conclusion: These results suggest that Cd has direct detrimental effects on cell viability, MMPs activity and protease/anti-protease balance which may contribute to alveolar wall destruction and pulmonary diseases.

Open access

Ramin Tavakoli, Hamid Yaghooti, Robab Daghagheleh, Rohollah Yousofi and Parisa Rahimifar

Abstract

Background

Depression is a neuroprogressive disorder that is characterized by neurotransmitter derangement and decreased neurogenesis and neurotrophic factors including brain-derived neurotrophic factor (BDNF).

Objectives

To determine the lipid profiles and BDNF levels in university students at an institution in Iran and association of these factors with Beck Depression Inventory (BDI) scores.

Methods

We conducted an observational study of a cross-section of male students at the Ahvaz Jundishapur University of Medical Sciences in Iran. For each of the 100 participants, a BDI score was obtained and serum levels of BDNF were measured by enzyme-linked immunosorbent assay. Levels of serum lipids, including cholesterol, triglycerides, low-density lipoprotein (LDL), and high-density lipoprotein (HDL), were measured using a biochemical analyzer. Castelli’s risk index type I (CRI-I), Castelli’s risk index type II (CRI-II), CRI-I = TG/HDL-C and CRI-II = LDL-cholesterol/ HDL-cholesterol, and atherogenic index of plasma (AIP), AIP = log (triglycerides/HDL-cholesterol), were calculated.

Results

Based on BDI scores, lower levels of BDNF, triglycerides, cholesterol, and HDL, but higher levels of LDL were found in participants with higher BDI scores. CRI-I was also increased in participants with depression.

Conclusion

The levels of BDNF and lipid factors are associated with the severity of depression in Iranian male university students. Deranged levels of BDNF and lipids may predispose depressed students to cardiovascular diseases.

Open access

Hamid Yaghooti, Mohsen Firoozrai, Soudabeh Fallah and Mohammad Reza Khorramizadeh

Abstract

Background: Adenosine is known as a protective and anti-inflammatory nucleoside. Angiotensin II is the main hormone of the renin-angiotensin system. It is associated with endothelial permeability, recruitment, and activation of the immune cells through induction of inflammatory mediators. Matrix metalloproteinase-9 (MMP-9) plays an important role in inflammatory processes mediated by macrophages. Objectives: Investigate whether adenosine pretreatment modulates angiotensin II-induced MMP-9 expression and activation of signaling molecules. Methods: Human monocytic U-937 cells were treated with either adenosine or angiotensin II alone or angiotensin II following a pretreatment with adenosine. Supernatants were analyzed for MMP-9 activity by zymography method. MMP-9 gene expression was analyzed using real-time PCR. Activation of inflammatory mediators IκB-α, NF-κB, JNK, p38 MAPK, and STAT3 were analyzed by a multi-target ELISA kit. Association of Protein kinase A (PKA) in adenosine effects was studied by pre-incubation with H89, a selective PKA inhibitor. Results: Treatment of the cells with angiotensin II significantly increased MMP-9 production (p <0.05). Adenosine pretreatment did not attenuate this angiotensin II effect. Angiotensin II treatment induced NF-κB, JNK and p38 activation. Pretreatment with adenosine prior to angiotensin II stimulation showed a 40% inhibitory effect on p38 induction (p <0.05). This effect was reversed by PKA inhibition. Conclusion: The present data confirmed that monocytic MMP-9 was a target gene for angiotensin II. Adenosine pretreatment did not inhibit MMP-9 increase in response to angiotensin II. However, it showed a potential inhibitory effect on angiotensin II inflammatory signaling.