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1.
Int J Fertil Steril ; 16(3): 192-199, 2022 Aug 21.
Article in English | MEDLINE | ID: mdl-36029056

ABSTRACT

BACKGROUND: Aim of the study was to evaluate the protective effects of trans-anethole, against polycystic ovary syndrome (PCOS) induced histopathological and biochemical changes in female Wister rats.
Materials and Methods: In this experimental study, forty-eight animals were randomly assigned into 6 groups: control; PCOS; PCOS+trans-anethole (20, 40, 80 mg/kg); and PCOS+metformin (300 mg/kg). Testosterone (1 mg/kg/day) was injected intraperitoneally for 35 days to induce PCOS. After PCOS induction, animals were treated by transanethole and metformin (30 days oral gavage). Finally, serum oxidative stress and insulin levels as well as histological changes in ovaries, kidneys and liver were evaluated.
Results: In PCOS group, the serum level of malondialdehyde (MDA) was 1.391 ± 0.18 mmol/L and significantly
increased (P=0.000) compared to the control group with the MDA level of 0.35 ± 0.08. Meanwhile the activity of
superoxide dismutase (SOD) and catalase (CAT), and total thiol levels were significantly decreased (P=0.000 for all
groups), compared to the control group. In the trans-anethole (80 mg/kg) treated group, insulin (P=0.000) and MDA
(P=0.000) levels were significantly decreased while total thiol (P=0.001) and activity of SOD (P=0.000) and CAT
(P=0.007) were significantly increased compared to the PCOS group. In the metformin treated group the insulin level
(P=0.03) decreased compared to the PCOS group. Histological evaluation showed multiple cysts in the ovarian tissue,
an increase in inflammatory cells in the liver, and a loss of order in the structure of the tubules and glomeruli of the
kidney in the PCOS group. Tissue damage was reduced in the trans-anethole treated group.
Conclusion: Tarns-anethole at a dose of 80 mg/kg improved metabolic status, oxidative stress, liver and kidney damage
as well as the cystic mass of ovarian tissue. To understand the exact protective effects of trans-anethole in PCOS,
more experimental or clinical studies are suggested.

2.
Clin Exp Hypertens ; 44(7): 663-669, 2022 Oct 03.
Article in English | MEDLINE | ID: mdl-35972305

ABSTRACT

INTRODUCTION: Subclinical hyperthyroidism (SHT) is an endocrine disorder that is associated with abnormalities in heart structure and function. Oxidative stress plays an important role in the pathophysiology of cardiac disorders caused by SHT. Portulaca oleracea (P. Oleracea) is a herbaceous plant with many pharmacologic effects including antioxidant, and anti-inflammatory properties. In the present study, the effects of Portulaca oleracea and vitamin E on the biochemical, hemodynamic, and functional parameters of the cardiac tissue was studied in rats with subclinical hyperthyroidism. METHODS: Fifty-six male rats were divided into seven groups: 1-Control group: daily injection of saline, 2-SHT group: daily injection of levothyroxine sodium (LS) (20 µg/kg), 3- T4+Po groups were given LS and P. oleracea (100, 200, and 400 mg/kg in drinking water), 4- the T4+vit E groups received LS and a daily injection of vitamin E (100 and 200 mg/kg). Cardiac index, systolic blood pressure (SBP), also malondialdehyde and total thiol levels were measured in cardiac tissue. RESULTS: SBP and maximum dP/dt were significantly increased and minimum dP/dt was significantly decreased in SHT group. In P. oleracea groups, maximum dP/dt were significantly reduced and minimum dP/dt was increased. Malondialdehyde levels and cardiac index in groups receiving vitamin E and P. oleracea were significantly decreased. Maximum dP/dt was decreased in the group receiving LS+vitamin E. Minimum dP/dt was significantly higher in group received LS+ vitamin E. CONCLUSION: This study showed that Portulaca oleracea has a positive effect on cardiac dysfunction caused by subclinical hyperthyroidism.


Subject(s)
Hyperthyroidism , Portulaca , Animals , Malondialdehyde , Plant Extracts , Rats , Vitamin E
3.
Environ Sci Pollut Res Int ; 28(40): 56822-56834, 2021 Oct.
Article in English | MEDLINE | ID: mdl-34080114

ABSTRACT

Emphysema is associated with an abnormal airspace enlargement distal to the terminal bronchioles accompanied by destructive changes in the alveolar walls and chronic inflammation. Air pollution can cause respiratory diseases such as chronic obstructive pulmonary disease (COPD) and emphysema in urban areas. As a natural antioxidant compound, gallic acid may be effective in controlling inflammation and preventing disease progression. In this research, we investigated the protective role of gallic acid in the inflammatory process and the possible signaling pathway in the elastase-induced emphysema. Forty-eight rats were divided into six different groups including the following: control, gallic acid (7.5, 15, and 30 mg/kg), porcine pancreatic elastase (PPE), and PPE+gallic acid 30 mg/kg. Oxidative stress indexes such as malondialdehyde and antioxidant enzyme activity were measured in all groups. The gene expression levels of heme oxygenase-1 (HO-1), nuclear factor (erythroid-derived 2)-like 2 (Nrf2), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) were determined as key regulators of antioxidant and inflammation system. The PPE group showed pulmonary edema and a significant change in arterial blood gas values, which was associated with decreased antioxidant activity of enzymes and changes in NF-κB, HO-1, and Nrf2 gene expression in comparison to the control group. Co-treatment with gallic acid preserved all these changes approximately to the normal levels. The results confirmed that elastase-induced emphysema leads to lung injuries, which are associated with oxidative stress and inflammation. Also, the results suggested that gallic acid as a natural antioxidant agent can modulate the Nrf2 signaling pathway to protect the lung against elastase-induced emphysema. Therefore, we documented the evidence for the importance of NF-κB inhibitors and Nrf2 activators as a target for new treatments in respiratory dysfunction caused by oxidative agents.


Subject(s)
Emphysema , NF-E2-Related Factor 2 , Animals , Gallic Acid/pharmacology , Heme Oxygenase-1/genetics , Heme Oxygenase-1/metabolism , Inflammation/chemically induced , NF-E2-Related Factor 2/genetics , NF-E2-Related Factor 2/metabolism , NF-kappa B/genetics , NF-kappa B/metabolism , Oxidative Stress , Pancreatic Elastase , Rats , Signal Transduction , Swine
4.
Avicenna J Phytomed ; 11(1): 44-53, 2021.
Article in English | MEDLINE | ID: mdl-33628719

ABSTRACT

OBJECTIVE: Apium graveolens L. (celery) seed has been used for hypertension treatment. To provide a pharmacological basis, the vasorelaxant effect of celery seed extract was investigated in isolated rat aorta. MATERIALS AND METHODS: Wistar male rats (200-250 g) were divided into 15 groups (n=7 for each group). The vasorelaxant response of different concentrations of celery seed extract (0.05, 0.1, 0.25, 0.5, 1, and 2 mg/ml) on isolated aorta precontracted with phenylephrine (PE) or KCl was evaluated by organ bath technique. The role of endothelium, extracellular calcium influx, intracellular sources of calcium, and potassium channels in vasorelaxant effect of celery seed extract was investigated. RESULTS: The extract showed a concentration-dependent relaxation in the isolated aorta contracted with PE and KCl that was endothelium-dependent at lower concentrations. Pretreatment of aortic rings with indomethacin or L-NAME, did not affect the vasorelaxation induced by celery seed extract. The extract inhibited KCl and PE-induced contractions in cumulative calcium concentrations as well as after incubation with diltiazem in denuded aortic rings of endothelium. The relaxation induced by celery seed extract was inhibited by 4-aminopyridine. CONCLUSION: This relaxation was mediated by inhibiting calcium influx into vascular smooth muscle cells. Also, voltage-dependent potassium channels were involved in inducing the vasorelaxant effect of celery seed extract.

5.
Iran J Basic Med Sci ; 23(9): 1130-1138, 2020 Sep.
Article in English | MEDLINE | ID: mdl-32963734

ABSTRACT

OBJECTIVES: Cardiovascular disease has an important role in mortality caused by lung injury. Emphysema is associated with impaired pulmonary gas exchange efficiency and airflow limitation associated with small airway inflammation. The aim was to evaluate the interactions between lung injury, inflammation, and cardiovascular disease. Since gallic acid has antioxidant and anti-inflammatory effects, we hypothesized that gallic acid protects the lung and the related heart dysfunction in elastase-induced lung injury. MATERIALS AND METHODS: Forty-eight Sprague-Dawley male rats were randomly divided into six groups: Control, Porcine pancreatic elastase (PPE) , PPE+GA, and 3 groups for different doses of gallic acid (GA 7.5, GA 15, GA 30 mg/kg). PPE was injected intra-tracheally on days 1 and 10 of the test. In each group, electrocardiography, hemodynamic parameters, oxidative stress, and bronchoalveolar lavage fluid were examined. RESULTS: PPE administration showed a decrease in HR and QRS voltage of electrocardiogram parameters, as well as in hemodynamic parameters (P<0.05, P<0.01, and P<0.001) and superoxide dismutase (SOD) (P<0.05). Tumor Necrosis Factor α (TNF-α) (P<0.001), interleukin 6 (IL-6) (P<0.001), interleukin 6 (MDA) (P<0.001), and the total number of white blood cells (P<0.001) showed an increase in PPE groups. Gallic acid preserved the values of hemodynamic properties, oxidative stress, inflammation, and electrocardiogram parameters in comparison to the PPE group. CONCLUSION: Briefly, this study showed the valuable effect of gallic acid in cardiac dysfunction related to elastase-induced lung injury. These findings suggested that gallic acid, as a natural antioxidant, has a potential therapeutic effect on preventing oxidative stress, inflammation, and subsequent cardiovascular disease.

6.
Life Sci ; 256: 117848, 2020 Sep 01.
Article in English | MEDLINE | ID: mdl-32585243

ABSTRACT

AIM: Pulmonary arterial hypertension (PAH) identified by progressive increase in pulmonary vascular resistance and pressure, ultimately leading to right ventricular failure and sudden death. Oxidation resistance 1 (OXR1) and its downstream target genes has a pivotal role for defense against oxidative stress. But its molecular function is unknown in respiratory system disorders. This study designed to determine whether PAH associated with oxidative stress and OXR1 signaling pathway modulation. Also, Crocin co-treatment evaluated to determine the possible role and mechanism in pulmonary arterial hypertension. MAIN METHOD: The PAH model was induced by a single dose of MCT. It was given intraperitoneal administration of Crocin or saline for 21 consecutive days the other groups in this study. In the last day of experiment, hemodynamic parameter and right ventricular hypertrophy was evaluated as PAH index. The expression levels of OXR1, P21 and Nrf2 genes were detected through RT-PCR. Moreover, oxidative stress index and antioxidant capacity were measured and histological examination were used to determine the lung tissue injuries. KEY FINDINGS: Results of the current study demonstrated that the OXR1 and P21 gene expression significantly decrease in PAH which is associated with increase of lipid peroxidation and decrease antioxidant capacity in lung tissue. Crocin co-treatment significantly improved the hemodynamic, oxidative stress biomarkers and histological data of the PAH rats, which associated with increase of OXR1 and its downstream target genes. SIGNIFICANCE: This report reveals the critical role of OXR1 in pathogenesis of oxidative stress-related pulmonary disease. Current experiment also provides evidence that Crocin has a protective effect against MCT-induced pulmonary arterial hypertension by modulation of OXR1 signaling pathway in rats.


Subject(s)
Carotenoids/pharmacology , Hypertrophy, Right Ventricular/physiopathology , Oxidative Stress/drug effects , Pulmonary Arterial Hypertension/prevention & control , Animals , Antioxidants/metabolism , Disease Models, Animal , Gene Expression Regulation , Lipid Peroxidation/physiology , Male , Mitochondrial Proteins/genetics , Mitochondrial Proteins/metabolism , Monocrotaline/toxicity , Oxidative Stress/physiology , Pulmonary Arterial Hypertension/genetics , Pulmonary Arterial Hypertension/physiopathology , Rats , Rats, Sprague-Dawley , Reactive Oxygen Species/metabolism , Signal Transduction/drug effects
7.
J Diet Suppl ; 15(5): 715-727, 2018 Sep 03.
Article in English | MEDLINE | ID: mdl-29172882

ABSTRACT

We investigated the effects of feeding vitamin C (Vit C) during neonatal and juvenile growth on learning and memory of rats. Rats after delivery were randomly divided into four groups and treated. Group 1, control group, received normal drinking water. Groups 2-4 received Vit C 10, 100, and 500 mg/kg, respectively, from the first day. After 8 weeks, 10 male offspring of each group were randomly selected and tested in the Morris water maze (MWM) and passive avoidance (PA) tests. Finally, the brains were removed for biochemical measurement. In MWM, 10-500 mg/kg Vit C reduced the latency and traveled distance and increased time spent in the target quadrant. In PA, 10 and 100 mg/kg of Vit C increased the latency; 10-500 mg/kg of Vit C decreased the malondialdehyde (MDA) in the brain tissues and increased thiol and catalase (CAT) activity compared to the control group. We showed that feeding rats Vit C during neonatal and juvenile growth has positive effects on learning and memory.


Subject(s)
Animals, Newborn/growth & development , Ascorbic Acid/administration & dosage , Learning/drug effects , Memory/drug effects , Animals , Avoidance Learning/drug effects , Brain/drug effects , Brain Chemistry/drug effects , Catalase/analysis , Diet , Female , Male , Malondialdehyde/analysis , Maze Learning/drug effects , Pregnancy , Rats , Rats, Wistar , Sulfhydryl Compounds/analysis
8.
Int J Prev Med ; 9: 110, 2018.
Article in English | MEDLINE | ID: mdl-30687461

ABSTRACT

BACKGROUND: Diabetes mellitus (DM) is a prime risk factor for cardiovascular disease. The convincing experimental and clinical evidence indicated that the onset of DM is closely associated with oxidative stress and that the generation of reactive oxygen species increases in both the types of diabetes. The aim of the present study was to evaluate the effect of Teucrium polium (TP) hydroalcoholic extract on the blood glucose, cholesterol, triglyceride, and oxidative stress markers of the heart and aorta in streptozotocin (STZ)-induced diabetic rats. METHODS: The male Wistar rats assigned into six groups (n = 8 in each group): Control, diabetic, and diabetic rats treated with TP extract (100, 200, and 400 mg/kg) or met and metformin (300 mg/kg) formin (300 mg/kg) group, by daily gavage for 6 weeks. Diabetes was induced by injection of STZ (60 mg/kg, i.p). Serum lipids and glucose, malondialdehyde (MDA) level, total thiol level, and also the activities of Cu, Zn-superoxide dismutase (SOD) in the cardiac and aortic tissues were assessed. RESULTS: TP extract reduced serum glucose, triglyceride and cholesterol. The MDA levels were reduced significantly in all TP-treated groups and metformin. Total thiol levels were improved in the heart and aorta of TP extract-treated groups and metformin compared to the diabetic rats. The activity of SOD in the cardiac and aortic tissues of TP extract- and metformin-treated groups was higher than diabetic group. CONCLUSIONS: The results showed that chronic administration of TP in STZ-induced diabetic rats could decrease blood glucose, cholesterol, and triglyceride and also attenuate the oxidative stress in the aortic and cardiac tissues.

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