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1.
Medicina (Kaunas) ; 55(7)2019 Jul 23.
Artigo em Inglês | MEDLINE | ID: mdl-31340610

RESUMO

Background and Objectives: Several studies have reported that some conditions such as exercise and hypoxia induce DNA damage and dysfunction and apoptosis. Some plant foods contain numerous bioactive compounds and anti-inflammatory properties that can help fight DNA damage. Therefore, the current study evaluated the effect of supplementation of Adiantum capillus-veneris (ACV) extract on Bax/B-cell lymphoma 2 (Bcl-2) ratio apoptotic index and remodeling of pulmonary alveolar epithelial cells in lung tissue of healthy Wistar rats during stressful conditions (hypoxia). Materials and Methods: Twenty-seven Wistar male rats (four-week old, 72 ± 9 g) were randomly assigned into three groups: normoxic, sedentary, and not-supplemented (NG, n = 9); exercise and hypoxia and not-supplemented (HE, n = 9); and exercise and hypoxia and supplemented group (HS, n = 9). The NG remained sedentary in the normoxia environment for nine weeks. The HE group participated in a high-intensity (IT) program for six weeks, then remained sedentary in the hypoxia environment for three weeks. The low-pressure chamber simulated a ~2800 M altitude 24 h/d. HS participated in IT, then entered and remained sedentary in the hypoxia environment for three weeks, and they consumed 500 mg per kg of body weight ACV extract. Results: The Bax/Bcl-2 ratio of the HE group increased significantly (+50.27%, p ≤ 0.05), the average number of type I pneumocytes was reduced significantly (-18.85%, p ≤ 0.05), and the average number of type II pneumocytes was increased significantly (+14.69%, p ≤ 0.05). Also, after three weeks of consuming the ACV extract, the HS group in comparison with the HE group had their Bax/Bcl-2 ratio reduced significantly (-24.27%, p ≤ 0.05), the average number of type I pneumocytes increased significantly (+10.15%, p ≤ 0.05), and the average number of type II pneumocytes reduced significantly (-7.18%, p ≤ 0.05). Conclusion: The findings show that after three weeks of hypoxia following six weeks of high-intensity interval training in Wistar rats, the Bax/Bcl-2 ratio and the number of type II pneumocytes were increased and the number of type I pneumocytes was reduced significantly. These results strongly suggest that an apoptosis state was induced in the lung parenchyma, and consuming ACV extract modulated this state.


Assuntos
Adiantum/metabolismo , Apoptose/efeitos dos fármacos , Terapia por Exercício/normas , Hipóxia/tratamento farmacológico , Extratos Vegetais/uso terapêutico , Alvéolos Pulmonares/efeitos dos fármacos , Animais , Modelos Animais de Doenças , Terapia por Exercício/métodos , Hipóxia/fisiopatologia , Extratos Vegetais/farmacologia , Alvéolos Pulmonares/fisiopatologia , Ratos , Ratos Wistar
2.
Vet Res Forum ; 11(2): 143-152, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32782743

RESUMO

The present study aimed to investigate the protective effect of silymarin on maternal cadmium toxicity complications in the kidney of neonatal rats. Forty adults Wistar female rats were selected and placed with male rats for copulation. The pregnant animals were randomly divided into five groups (n = 8) including control, sham, silymarin, cadmium, and silymarin + cadmium. The animals received 400 mg L-1 cadmium and 100 mg kg-1 silymarin (sub-cutaneously, three days per week, three weeks). Two-day neonates were dissected and their right kidneys were fixed in 10.00% buffered formalin solution and processed by standard paraffin embedding. Tissue sections were stained by hematoxylin and eosin and analyzed histologically and stereologically. The data were statistically analyzed by SPSS using a one-way ANOVA test and Tukey's post-hoc. The results showed that silymarin significantly increased the neonatal rats' weight compared to the control group. Cadmium significantly decreased the weight of neonatal rats' kidneys. The results of histological studies indicated that cadmium caused subacute glomerulosclerosis, severe damage to urinary tubules such as tubular necrosis, and severe hyperemia in the medulla, but silymarin could preserve these complications. Stereological results revealed that cadmium decreased the total volume of kidney, medulla, and proximal and distal tubules and increased interstitial tissue and indicated the protective effects of silymarin on maternal cadmium toxicity complications in the kidney tissue of neonatal rats. It can be concluded that the administration of silymarin during pregnancy may be used as a useful and effective way of protecting the maternal cadmium toxicity complications in the kidney tissue of neonatal rats.

3.
Adv Respir Med ; 87(4): 226-234, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31476010

RESUMO

INTRODUCTION: Evidence suggests that hypoxia and high-intensity exercise training can increase apoptosis of lung cells and Adiantum capillus-veneris (Ac-v) extract can have anti-apoptotic effects. Thus, the aim of the present study was to investigate the effect of chronic hypoxia and the (Ac-v) extraction as a supplement on TNF-a and P53 protein expression as well as the respiratory surface. MATERIAL AND METHODS: 24 healthy Wistar rats (age = 4 weeks, weight = 72 = 9 gr) were trained using interval training for 6 weeks followed by a 3-week stay in hypoxia conditions. Half of the hypoxia samples received 500 ml/gr/per body weight daily (Ac-v) within 3 weeks of hypoxia. At the end, the lung tissue was removed for histological and immunohistological analysis. RESULTS: After 3 weeks of hypoxia exposure following 6 weeks of exercise, expression of P53 and TNF-a increased and the respiratory surface decreased (p ≤ 0.05). After 3 weeks of taking the Ac-v extract during hypoxia exposure, reduced P53 and TNF-a expression and the increased respiratory surface were observed (p ≤ 0.05). CONCLUSIONS: Chronic hypoxia may be considered as a strong stimulus leading to the expression of proteins involved in apoptosis and tissue disruption. However, our findings suggest that the antioxidative properties of Ac-v extract could decrease the destructive structural and molecular events that happen along with hypoxia exposure or intense exercise training.


Assuntos
Adiantum , Antioxidantes/uso terapêutico , Hipóxia/tratamento farmacológico , Fitoterapia/métodos , Extratos Vegetais/uso terapêutico , Proteína Supressora de Tumor p53/efeitos dos fármacos , Animais , Antioxidantes/farmacologia , Masculino , Extratos Vegetais/farmacologia , Ratos , Ratos Wistar , Proteína Supressora de Tumor p53/metabolismo
4.
Caspian J Intern Med ; 9(2): 158-163, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29732034

RESUMO

BACKGROUND: Tobacco contains carcinogens such as NNK (nicotine-derived nitrosamine ketone) that makes induction of lung cancer by changing the stimulation of IL-10 expression. The aim of this study was to investigate changes in resting levels of IL-10 in lung tissues of rats exposed to NNK after a 12-week aerobic submaximal swimming training. METHODS: For this purpose, 46 Wistar rats were randomly divided into five groups consisting training, training + NNK, NNK, saline and control. NNK-induced groups received NNK subcutaneously one day per week at a rate of 12/5 mg per kg body weight and the training groups performed submaximal swimming training for 12 weeks. The levels of IL-10 in homogenized lung tissue were measured by ELISA. RESULTS: Findings indicated that a period of swimming training increased the IL-10 levels significantly in lung tissue of training group when compared to control (P=0.00) and NNK groups (P=0.00). Also, a significant increase of IL-10 level was observed in exercise + NNK group when compared to NNK group (p≤0/02). Furthermore, it was observed that IL-10 levels of NNK group had a significant decrease when compared to training group (P=0/00), training + NNK group (p≤0/02), but had insignificant increase when compared to saline group (p≤0/85). CONCLUSIONS: Generally, it could be confirmed that regular submaximal aerobic training plays an important role in the inhibition of the effects of lung inflammation induced by NNK via increasing IL-10 activity.

5.
Iran J Allergy Asthma Immunol ; 17(5): 418-427, 2018 Oct 07.
Artigo em Inglês | MEDLINE | ID: mdl-30518184

RESUMO

The nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK; nicotine derived nitrosamine ketone) is one of the strongest carcinogens in tobacco which is involved in induction of lung cancer by changing the stimulation of vascular endothelial growth factor (VEGF) and annexin A2 expression. The aim of this study was to investigate the changes in resting levels of annexin A2 and VEGF in lung tissues of rats exposed NNK after 12 weeks of aerobic submaximal swimming training. For this purpose, 46 Wistar rats were randomly divided into five groups consist of training, training + NNK, NNK, saline and control. NNK-induced groups received NNK subcutaneously one day per week at a rate of 12/5 mg per kg body weight and the training groups performed submaximal swimming training for 12 weeks. The levels of VEGF and annexin A2 in lung tissue were measured respectively by ELISA and immunohistochemistry. To analyze the data; ANOVA and Tukey's test were used at a significance level of p<0.05. Findings indicated that 12 weeks submaximal swimming training decreased the levels of VEGF and annexin A2 in lung tissue significantly when compared to NNK group (p<0.001). There was no significant correlation between VEGF and annexin A2 levels in all study groups (p≥0.05). Generally, it could be confirmed that regular submaximal aerobic training plays an important role in inhibition of the effects of lung inflammation induced by NNK via decreased levels of VEGF and annexin A2.


Assuntos
Anexina A2/metabolismo , Carcinógenos/toxicidade , Neoplasias Pulmonares/metabolismo , Pulmão/metabolismo , Nitrosaminas/toxicidade , Pneumonia/metabolismo , Fator A de Crescimento do Endotélio Vascular/metabolismo , Animais , Humanos , Imuno-Histoquímica , Pulmão/patologia , Neoplasias Pulmonares/induzido quimicamente , Condicionamento Físico Animal , Pneumonia/induzido quimicamente , Ratos , Ratos Wistar , Natação , Fumar Tabaco/efeitos adversos
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