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1.
Chonnam Medical Journal ; : 1-5, 2022.
Article in English | WPRIM | ID: wpr-913906

ABSTRACT

There is no denying that the massive spread of COVID-19 around the world has worried everyone. The virus can cause mild to severe symptoms in various organs, especially the lungs. The virus affects oxidative stress in the cells. Reactive Oxygen Species modulator 1 (ROMO1) is one of the most important mitochondrial proteins that plays a critical regulatory role in the production of Reactive Oxygen Species (ROS). According to the studies, COVID-19 can promote oxidative stress through some important pathways, for instance, TNF-α and NF-κB routes. Furthermore, ROMO1 is closely related to these pathways and its dysfunction may affect these routes, then promote oxidative stress, and ultimately cause tissue damage, especially in the lungs. Another factor to consider is that the TNF-α and NF-κB pathways are associated with ROMO1, COVID-19, and oxidative stress. To summarize, it is hypothesized that COVID-19 may increase oxidative stress by affecting ROMO1. Understanding the exact molecular mechanisms of ROMO1 in the pathogenesis of COVID-19 can pave the way to find better therapeutic strategies.

2.
Asian Pacific Journal of Tropical Biomedicine ; (12): 397-402, 2020.
Article in Chinese | WPRIM | ID: wpr-950278

ABSTRACT

Objective: To evaluate the effect of resveratrol against CCl

3.
Chonnam Medical Journal ; : 136-143, 2019.
Article in English | WPRIM | ID: wpr-763292

ABSTRACT

Today, the incidence of cancer in the world is rising, and it is expected that in the next several decades, the number of people suffering from cancer or (the cancer rate) will double. Cancer is defined as the excessive and uncontrolled growth of cells; of course (in simple terms), cancer is considered to be a set of other diseases that ultimately causes normal cells to be transformed into neoplastic cells. One of the most important causes of the onset and exacerbation of cancer is excessive oxidative stress. One of the most important proteins in the inner membrane of mitochondria is Reactive Oxygen Species (ROS) Modulator 1 (ROMO1) that interferes with the production of ROS, and with increasing the rate of this protein, oxidative stress will increase, which ultimately leads to some diseases, especially cancer. In this overview, we use some global databases to provide information about ROMO1 cellular signaling pathways, their related proteins and molecules, and some of the diseases associated with the mitochondrial protein, especially cancer.


Subject(s)
Diagnosis , Incidence , Membranes , Mitochondria , Mitochondrial Proteins , Oxidative Stress , Reactive Oxygen Species
4.
IJRM-International Journal of Reproductive Biomedicine. 2018; 16 (2): 93-100
in English | IMEMR | ID: emr-198542

ABSTRACT

Background: Neopterin is a significant and sensitive marker in estimating the activity of cellular immune system. Oxidative stress plays a role in the etiology of male infertility. Increased reactive oxygen species is accompanied with increase in neopterin level. Hence neopterin may be involved in male infertility


Objective: The objective of this case-control study was to determine neopterin level in idiopathic infertile and normospermic men; furthermore, to identify its relationship with oxidative stress markers including total oxidant, malondialdehyde, sperm DNA fragmentation, and total antioxidant capacity of seminal plasma


Materials and Methods: Forty seven infertile and forty three normospermic males were selected according to WHO criteria. Their semen and blood samples were taken; subsequently, the levels of neopterin, total oxidant, total antioxidant, malondialdehyde, and sperm DNA fragmentation were measured


Results: The levels of neopterin, total oxidant, and malondialdehyde in seminal plasma of infertile males were significantly higher than those of normospermic group [p=0.038, 0.018, and 0.028, respectively]. Furthermore, sperm DNA fragmentation in infertile men was higher than that of control group [p<0.001]. Moreover, total antioxidant capacity of seminal plasma in infertile males was significantly lower than that of normospermic subjects [p=0.002]. No significant difference was observed in serum neopterin, total oxidant, and malondialdehyde between the infertile and normospermic groups


Conclusion: The significant inverse correlation between seminal plasma neopterin and total antioxidant in the infertile males supports a possible role of neopterin in male infertility. Neopterin can be suggested as a marker in monitoring and diagnosis of idiopathic male infertility

5.
Chonnam Medical Journal ; : 118-126, 2017.
Article in English | WPRIM | ID: wpr-151395

ABSTRACT

Nilotinib as a tyrosine kinase inhibitor has been recently used to improve the liver fibrosis process, but the exact mechanisms still require further clarification. In this study, we investigated the anti-fibrotic effects of Nilotinib via RAGE/HMGB1axis and antioxidant mechanisms. This experimental study was performed in the Hamadan University of Medical Sciences, Iran, from May 2015 to December 2016. Liver fibrosis was induced in Wistar male rats by CCL₄. Rats were gavaged daily with Nilotinib (10 mg/kg). RAGE, HMGB1, TNF-α and TGF-β mRNA expression were evaluated by quantitative RT-PCR. TNF-α protein levels were measured using the immunoassay method. Thiol groups, carbonyl groups, nitric oxide levels and glutathione peroxidase activity were measured by spectrophotometric methods.The results showed that Nilotinib decreased TNF-α, TGF-β, RAGE and HMGB1 mRNA expression (p<0.001) in the liver tissues of the fibrosis group. Nilotinib also decreased carbonyl groups and nitric oxide levels and increased thiol groups and glutathione peroxidase activity in the fibrosis groups. The histopathological changes were found to be attenuated by Nilotinib. In conclusion, Nilotinib can improve liver fibrosis and open new mechanisms of the anti-fibrotic properties of Nilotinib.


Subject(s)
Animals , Humans , Male , Rats , Fibrosis , Gene Expression , Glutathione Peroxidase , HMGB1 Protein , Immunoassay , Iran , Liver Cirrhosis , Liver , Methods , Nitric Oxide , Oxidative Stress , Protein-Tyrosine Kinases , Rage , RNA, Messenger
6.
Chonnam Medical Journal ; : 118-126, 2017.
Article in English | WPRIM | ID: wpr-788375

ABSTRACT

Nilotinib as a tyrosine kinase inhibitor has been recently used to improve the liver fibrosis process, but the exact mechanisms still require further clarification. In this study, we investigated the anti-fibrotic effects of Nilotinib via RAGE/HMGB1axis and antioxidant mechanisms. This experimental study was performed in the Hamadan University of Medical Sciences, Iran, from May 2015 to December 2016. Liver fibrosis was induced in Wistar male rats by CCL₄. Rats were gavaged daily with Nilotinib (10 mg/kg). RAGE, HMGB1, TNF-α and TGF-β mRNA expression were evaluated by quantitative RT-PCR. TNF-α protein levels were measured using the immunoassay method. Thiol groups, carbonyl groups, nitric oxide levels and glutathione peroxidase activity were measured by spectrophotometric methods.The results showed that Nilotinib decreased TNF-α, TGF-β, RAGE and HMGB1 mRNA expression (p<0.001) in the liver tissues of the fibrosis group. Nilotinib also decreased carbonyl groups and nitric oxide levels and increased thiol groups and glutathione peroxidase activity in the fibrosis groups. The histopathological changes were found to be attenuated by Nilotinib. In conclusion, Nilotinib can improve liver fibrosis and open new mechanisms of the anti-fibrotic properties of Nilotinib.


Subject(s)
Animals , Humans , Male , Rats , Fibrosis , Gene Expression , Glutathione Peroxidase , HMGB1 Protein , Immunoassay , Iran , Liver Cirrhosis , Liver , Methods , Nitric Oxide , Oxidative Stress , Protein-Tyrosine Kinases , Rage , RNA, Messenger
7.
IJRM-International Journal of Reproductive Biomedicine. 2015; 13 (12): 787-792
in English | IMEMR | ID: emr-174917

ABSTRACT

Background: Oxidative stress in reproductive system leads to sperm DNA damage and sperm membrane lipid peroxidation and may play an important role in the pathogenesis of male infertility, especially in idiopathic cases. Antioxidants such as carotenoids function against free radical damages


Objective: The aim of this study was to determine the levels of lycopene, beta-carotene and retinol in serum and their relationship with sperm DNA damage and lipid peroxidation in infertile and normospermic males


Materials and Methods: Sixty two infertile men and 71 normospermic men participated in this study. Blood and semen samples were collected from all subjects. Sperm DNA damage was measured using TUNEL method. Carotenoids, retinol, and malonedildehyde in serum were also determined


Results: DNA fragmentation was higher in infertile group comparing to control group. Serum levels of lycopene, beta-carotene and, vitamin A in infertile men were significantly lower than normospermic men [p< 0.001, =0.005, and =0.003 respectively]. While serum MDA was not significantly different between two groups, MDA in seminal plasma of infertile men was significantly higher than control group [p< 0.001]


Conclusion: We concluded that lycopene, beta-carotene, and retinol can reduce sperm DNA fragmentation and lipid peroxidation through their antioxidant effect. Therefore the DNA fragmentation assay and determination of antioxidants factors such as lycopene, beta-carotene and retinol, along with sperm analysis can be useful in diagnosis and treatment of men with idiopathic infertility

8.
Chonnam Medical Journal ; : 115-119, 2015.
Article in English | WPRIM | ID: wpr-87793

ABSTRACT

Betatrophin is a newly characterized circulating hormone that is produced in tissues such as adipose tissue and liver and stimulates pancreatic beta-cell proliferation. The purpose of the current study was to examine circulating betatrophin levels in Iranian patients with type 2 diabetes mellitus (T2DM) and in normal controls. Seventy-five subjects were enrolled in this case-control study in the following two groups: T2DM patients (n=40) and a group of age-, sex-, and BMI-matched normal control subjects (n=35). Circulating betatrophin concentrations as well as the blood lipid profile, body mass index (BMI), fasting blood sugar (FBS), glycated hemoglobin (HbA1c), and insulin resistance were determined. Circulating betatrophin levels were significantly higher in patients with T2DM than in the normal subjects (4.79+/-1.53 ng/mL vs. 2.79+/-1.11 ng/mL respectively; p=0.001). Serum triacylglycerol and total cholesterol were also significantly higher in patients with T2DM than in the control group. In the patients with T2DM, serum betatrophin was positively correlated with age, FBS, TG, total cholesterol, and HbA1c. The results of this initial study in Iran have shown that circulating betatrophin levels are significantly increased in Iranian patients with T2DM compared with a control group. Additionally, it is postulated that betatrophin as a novel hormone may be involved in the generation of an atherogenic lipid profile.


Subject(s)
Humans , Adipose Tissue , Blood Glucose , Body Mass Index , Case-Control Studies , Cholesterol , Diabetes Mellitus , Diabetes Mellitus, Type 2 , Fasting , Glycated Hemoglobin , Insulin Resistance , Iran , Liver , Triglycerides
9.
Chonnam Medical Journal ; : 115-119, 2015.
Article in English | WPRIM | ID: wpr-788321

ABSTRACT

Betatrophin is a newly characterized circulating hormone that is produced in tissues such as adipose tissue and liver and stimulates pancreatic beta-cell proliferation. The purpose of the current study was to examine circulating betatrophin levels in Iranian patients with type 2 diabetes mellitus (T2DM) and in normal controls. Seventy-five subjects were enrolled in this case-control study in the following two groups: T2DM patients (n=40) and a group of age-, sex-, and BMI-matched normal control subjects (n=35). Circulating betatrophin concentrations as well as the blood lipid profile, body mass index (BMI), fasting blood sugar (FBS), glycated hemoglobin (HbA1c), and insulin resistance were determined. Circulating betatrophin levels were significantly higher in patients with T2DM than in the normal subjects (4.79+/-1.53 ng/mL vs. 2.79+/-1.11 ng/mL respectively; p=0.001). Serum triacylglycerol and total cholesterol were also significantly higher in patients with T2DM than in the control group. In the patients with T2DM, serum betatrophin was positively correlated with age, FBS, TG, total cholesterol, and HbA1c. The results of this initial study in Iran have shown that circulating betatrophin levels are significantly increased in Iranian patients with T2DM compared with a control group. Additionally, it is postulated that betatrophin as a novel hormone may be involved in the generation of an atherogenic lipid profile.


Subject(s)
Humans , Adipose Tissue , Blood Glucose , Body Mass Index , Case-Control Studies , Cholesterol , Diabetes Mellitus , Diabetes Mellitus, Type 2 , Fasting , Glycated Hemoglobin , Insulin Resistance , Iran , Liver , Triglycerides
10.
IJPR-Iranian Journal of Pharmaceutical Research. 2014; 13 (1): 253-262
in English | IMEMR | ID: emr-136452

ABSTRACT

Anti-oxidant effects of propofol [2, 6-diisopropylphenol] were evaluated agains carbon tetrachloridet CCl[4] -induced oxidative stress in rat liver. 30 male rats were equally divided in to 6 groups [5 rats each]. Group I [control], while Group II was given CCl[4] [3 mL /Kg/day, IP]. Animals of Groups III received only propofol [10 mg/Kg/day, IP]. Group IV was given propofol+ CCl[4]. Group V was administered vitamin E [alpha-tocopherol acetate 15 mg/Kg/day, SC] .Animals of Group VII received alpha-tocopherol acetate + CCl[4] once daily for two weeks. After treatment, blood and liver mitochondria were isolated. Anti-oxidant enzymes activity such as glutathione peroxidase [GPx], superoxide dismutase [SOD] and oxidative stress marker such as reduced glutathione [GSH] and lipid peroxidation [LPO] concentration were measured. Oxidative stress induced with CCl[4] in liver mitochondria was evident by a significant increase in enzymatic activities of GPx, SOD, and LPO and decreased of GSH and vailability of mitochondria. Propofol and vitamin E restored CCl[4]-induced changes in GSH, GPx, SOD and LPO in blood and liver mitochondria. CCl[4] decreased viability of mitochondria that was recovered by propofol and vitamin E. It is concluded that oxidative damage is the mechanism of toxicity of CCl[4] in the mitochondria that can be recovered by propofol comparable to vitamin E

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