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1.
Ultrastruct Pathol ; 48(3): 153-171, 2024 May 03.
Artigo em Inglês | MEDLINE | ID: mdl-38654519

RESUMO

BACKGROUNDS: Chronic kidney disease (CKD) is a global public health problem. All progressive chronic kidney disease (CKD) is characterized by tubulointerstitial fibrosis. Exposure to high concentrations of carbon tetrachloride (including vapor) can destroy the kidneys. Autophagy played an important role in maintaining the homeostasis of organs. Impaired autophagy was frequently associated with renal damage and fibrosis. Recent data suggests that metformin protects against a variety of kidney disorders. AIM: To investigate the protective role of metformin on carbon tetrachloride induced renal damage via autophagy pathway. MATERIALS AND METHODS: Forty adult male albino rats were divided into four equal groups (10 rats, each); Group 1: control group. Group 2: olive oil group received olive oil 1.5 mg/kg twice weekly S.C for 12 weeks. Group 3: The ccl4 group, the rats were received ccl4 1.5 mg/kg twice weekly S.C for 12 weeks. Group 4: CCL4 and Metformin group received concomitant treatment of CCL4, 1.5 mg/kg twice weekly S.C and 100 mg/kg/day Metformin orally for 12 weeks. After sacrifice, kidneys were taken from all animal groups and processed for light and electron microscopy, immunological studies and biochemical tests. Statistical analysis was done. RESULTS: Administration of ccl4 resulted in histopathological changes in the kidney tissue in the form of areas of tissue destruction, inflammatory cell infiltration, congestion and fibrosis. Ultrastructurally, irregular thickening of GBM was observed. Improvement was noticed with concomitant treatment of ccl4 with metformin. CONCLUSION: Metformin administration can modulate histological and biochemical effects in the renal tissue induced by of ccl4.


Assuntos
Autofagia , Tetracloreto de Carbono , Fibrose , Rim , Metformina , Animais , Metformina/farmacologia , Masculino , Autofagia/efeitos dos fármacos , Ratos , Tetracloreto de Carbono/toxicidade , Rim/patologia , Rim/efeitos dos fármacos , Rim/ultraestrutura , Insuficiência Renal Crônica/patologia , Insuficiência Renal Crônica/tratamento farmacológico
2.
Tissue Cell ; 79: 101961, 2022 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-36327569

RESUMO

Multiple organ toxicity has been associated with cisplatin (CIS) treatment, limiting its clinical use. The human prostate and seminal vesicles are accessory sex organs with androgen-dependent morphogenesis, growth, and secretion. The present study aimed to investigate, for the first time, the toxic effect of CIS on normal prostate and seminal vesicles in the presence and absence of diosmin (DS). The animals were randomized into 4 groups as follows: control (received vehicle), CIS group (7.5 mg/kg, i.p. on 5th and 12th day), DS group (100 mg/kg, p.o. for 15 days), and DS+CIS group. Histopathological and biochemical analyses were conducted to elucidate the goal of this study. CIS administration significantly induced prostate and seminal vesicle toxicity as evidenced by alteration of serum testosterone, LH, FSH, PSA, steroidogenic HSD17B6 as well as seminal analysis markers. Remarkably, marked histopathological changes in thin and ultrathin structures were observed. Besides, CIS significantly boosted oxidative stress as evidenced by the up-regulation of MDA and down-regulation of TAC. CIS significantly induced tissue apoptosis concomitant with suppression of cellular proliferation and stem cell expression as indicated by up-regulation of activated caspase-3 and Bax expression along with down-regulation of Bcl-2, Ki67, and CD44 expression. Interestingly, DS fixed all disturbances in the prostate and seminal vesicles induced by CIS. Together, CIS could cause prostate and seminal vesicle toxicity by affecting hormonal, steroidogenic, oxidative stress, apoptosis, and proliferation processes, and this effect was reversed by DS administration.


Assuntos
Diosmina , Glândulas Seminais , Animais , Humanos , Masculino , Cisplatino/toxicidade , Próstata , Estresse Oxidativo , Apoptose
3.
Mol Cell Endocrinol ; 503: 110700, 2020 03 01.
Artigo em Inglês | MEDLINE | ID: mdl-31904405

RESUMO

Genetic and epigenetic factors contribute equally to the pathogenesis of type 1 diabetes mellitus. Sodium butyrate (NaB) has been reported to improve glucose homeostasis by modulation of the p38/ERK MAPK pathway. This work aims to evaluate the effect of NaB on the ultrastructure of pancreatic ß-cells and the PI3/AKT pathway. Juvenile albino male rats were used to establish a type 1 diabetes model using streptozotocin injection and NaB in a pre- and post-treatment schedule. Plasma glucose, insulin levels, and glucose tolerance were evaluated. Light and electron microscopy and immunohistochemistry were performed using Ki-67, caspase-3, and insulin. NaB treatment resulted in a significant improvement in plasma glucose levels, plasma insulin levels/expression, and ameliorated diabetes-induced histological alternations. Additionally, it increased the expression of phosphorylated AKT. These findings provide evidence that NaB may be useful in the treatment of juvenile diabetes.


Assuntos
Ácido Butírico/farmacologia , Diabetes Mellitus Experimental , Inibidores de Histona Desacetilases/farmacologia , Células Secretoras de Insulina/efeitos dos fármacos , Insulina/metabolismo , Animais , Ácido Butírico/uso terapêutico , Diabetes Mellitus Experimental/tratamento farmacológico , Diabetes Mellitus Experimental/metabolismo , Diabetes Mellitus Experimental/patologia , Diabetes Mellitus Tipo 1/tratamento farmacológico , Diabetes Mellitus Tipo 1/metabolismo , Diabetes Mellitus Tipo 1/patologia , Glucose/metabolismo , Inibidores de Histona Desacetilases/uso terapêutico , Resistência à Insulina , Secreção de Insulina/efeitos dos fármacos , Células Secretoras de Insulina/metabolismo , Células Secretoras de Insulina/patologia , Células Secretoras de Insulina/ultraestrutura , Masculino , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Ratos , Transdução de Sinais/efeitos dos fármacos
4.
Eur. j. anat ; 19(1): 15-26, ene. 2015. ilus
Artigo em Inglês | IBECS | ID: ibc-133886

RESUMO

The main objective of this study was to investigate the morphological aspects of the development of the Harderian gland (HG) in the female guinea pig. A total number of thirty animals were used and divided according to age into groups, five animals each. Specimens were taken at the following ages; birth, one week, two weeks, three weeks, four weeks and two months postnatal. Histological, histochemical and immunohistochemical techniques were used. The gland was constituted of secretory end pieces and a duct system formed of intra- and extra-parenchymal ducts. At birth, the female guinea pig HG was active in the secretion of lipid and neutral mucin and the differentiation of several populations of cells (light and dark) was possible. However, its histological structure was still incomplete. The lining cells revealed many free ribosomes, a few and small organelles and large irregularly shaped nuclei and numerous mitotic figures. The secretory cells reached maturity by the age of three weeks, but growth in size continued up to the age of two months. They were light or dark; the light cells presented three forms that exhibited different morphological features. All modes of secretion (apocrine, merocrine and holocrine) were detected


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Assuntos
Animais , Cobaias/crescimento & desenvolvimento , Glândula de Harder/crescimento & desenvolvimento , Glândula de Harder/anatomia & histologia , Microscopia de Polarização/métodos , Glândula de Harder/ultraestrutura
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