Atossa Jozaei; Monireh Movahedi; Maryam Khosravi; Fereshteh Golab
Volume 21, Issue 12 , 2019, Pages 1-8
Abstract
Background: Apoptosis is a programmed cell death that occurs due to various factors such as reperfusion ischemia. As a purinergic receptor, A1AR acts as an oxidative stress sensor and an antioxidant during reperfusion ischemia.Objectives: The purpose of the present study was to investigate the effect ...
Read More
Background: Apoptosis is a programmed cell death that occurs due to various factors such as reperfusion ischemia. As a purinergic receptor, A1AR acts as an oxidative stress sensor and an antioxidant during reperfusion ischemia.Objectives: The purpose of the present study was to investigate the effect of adenosine injection following cerebral reperfusion ischemia on A1AR gene expression and apoptosis in the brain hippocampal tissue of male Wistar rats.Methods: This experimental study was conducted at Shahid Mirghani Research Institute in Gorgan, Iran, from January 21, 2019, to March 18, 2019. The sample size was determined according to previous studies and a pilot study. Thus, 30 male Wistar rats were divided into three groups by simple random sampling (using a random-number table): Control group (n = 10), Reperfusion ischemia group (n = 10), and Reperfusion ischemia + adenosine group (n = 10). Ischemia was induced in animals by closing the carotid artery for 45 min. Adenosine was injected 24 h after ischemia. We measured A1AR gene expression, SOD protein expression, and apoptosis by real-time PCR, immunohistochemistry, and the TUNEL method, respectively.Results: The results showed that cerebral reperfusion ischemia significantly increased A1AR gene expression (596%) and apoptosis (378%) and decreased SOD protein expression (72%) compared to the control group (P < 0.001). On the other hand, adenosine sig- nificantly reduced A1AR gene expression (46%) and apoptosis (69%) and increased SOD protein expression (94%) compared to the ischemic group (P < 0.001).Conclusions: Ischemic brain reperfusion causes oxidative stress. Also, adenosine injection seems to be effective in reducing oxida- tive stress and apoptosis induced by cerebral reperfusion ischemia.
Nazila Amini; Monireh Movahedi; Ali Akbar Abolfathi; Ahmad Majd
Volume 20, Issue 6 , 2018, Pages 1-6
Abstract
Background: Helicobacter pylori (H. pylori) plays the primary role in increasing oxidative stress and causing stomach inflammation, peptic ulcers, and gastric malignancy in the infected patients. L-arginine (Arg) has antibacterial and anti-inflammatory effects. Objectives: The current study aimed at ...
Read More
Background: Helicobacter pylori (H. pylori) plays the primary role in increasing oxidative stress and causing stomach inflammation, peptic ulcers, and gastric malignancy in the infected patients. L-arginine (Arg) has antibacterial and anti-inflammatory effects. Objectives: The current study aimed at investigating the beneficial effects of L-arginine on inflammation and oxidative stress in patients infected with H. pylori with dyspeptic symptoms.Methods: The current randomized, double-blind controlled, clinical trial was conducted on 34 patients with H. pylori infection re- ferred to the center of digestive disorders affiliated to Isfahan University of Medical Sciences, Isfahan, Iran, in order to undergo en- doscopy from December 2016 to September 2017. Patients were classified into two groups (control and treatment); the control group only received triple-drug therapy (including Amoxicillin, Clarithromycin, and Omeprazole), and the treatment group received stan- dard triple-drug therapy and L-Arg capsules for three weeks. Gastric biopsies and serum samples were taken from all patients beforeand after the study. H. pylori infection was examined by a rapid urease test and antioxidant indices including superoxide dismutase (SOD), glutathione peroxidase (GPX), and total antioxidant capacity (TAC) were evaluated in gastric biopsies. In addition, serum samples were used to measure the inflammation factors including interleukin (IL)-8 and tumor necrosis factor (TNF)-α. Results: Level of SOD activity increased significantly in the treatment group compared with that of the control group (4.91 ± 95.21 vs. 4.0 ± 44.11 IU/mg) (P = 0.001). In the treatment group, compared with the control group, the level of TAC increased significantly (0.35 ± 0.60 vs. 0.30 ± 0.9 mM/L) (P = 0.006) and the level of GPX activity increased significantly in the treatment group compared with the control group (10.68 ± 2.39 vs. 5.16 ± 2.12 IU/mg) (P = 0.000). Regarding the inflammation factor, IL-8 decreased significantly in the treatment group compared with the control group (8.00 ± 1.94 vs. 10.28 ± 2.10 pg/mL) (P = 0.002); also TNF-α decreased significantly in the treatment group compared with the control group (9.71 ± 2.69 vs. 12.24 ± 3.29 pg/mL) (P = 0.036), while therewas no significant difference in high sensitivity C-reactive protein (hs-CRP) decrease between the treatment and the control groups (2.34 ± 1.28 vs. 3.04 ± 1.58 mg/L) (P = 0.16). Conclusions: Consumption of L-arginine increased antioxidant indices and decreased inflammation in patients infected with H. pylori.