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Medicinas Complementárias
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1.
J Mol Histol ; 53(3): 523-542, 2022 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-35118589

RESUMEN

Etoposide (Eto) is an anti-cancer drug that is associated with serious adverse effects on male reproductive function. Omega-3 polyunsaturated fatty acids (ω-3 PUFAs) and selenium (Se) are known as anti-inflammatory, anti-apoptotic and anti-oxidant agents. This work was designed to investigate changes in the biochemical parameters as well as alterations in Sertoli cell vimentin expression, ultrastructure and ectoplasmic specializations (ESs) following Eto treatment and to assess the ameliorative effect of ω-3 versus Se on these alterations. Eighty four adult male albino rats were used and classified into four groups: group I (control group), group II (Eto group) received Eto in a single intra-peritoneal (IP) dose (60 mg/kg B.W.), group III (Eto & ω-3 group) received the single IP dose of Eto as well as ω-3 (300 mg/kg B.W./day by intra-gastric intubation) starting 5 days before Eto injection till the time of sacrifice & group IV (Eto & Se group) received the single IP dose of Eto as well as Se (0.5 mg/kg B.W./day IP) starting 5 days before Eto injection till the time of sacrifice. The rats were subdivided into 2 subgroups (a) and (b) that were sacrificed 3 and 7 days after Eto injection respectively. Eto administration in group II induced increase in malondialdehyde (MDA), decrease in superoxide dismutase (SOD), collapse of Sertoli cell vimentin filaments and ultrastructural degenerative changes in both Sertoli cells and ESs. Se (group IV) reversed Eto toxic effects potently, while ω-3 (group III) had some limited protective effects.


Asunto(s)
Selenio , Células de Sertoli , Animales , Masculino , Electrones , Etopósido/metabolismo , Etopósido/farmacología , Selenio/metabolismo , Selenio/farmacología , Células de Sertoli/metabolismo , Testículo/metabolismo , Vimentina/metabolismo , Vimentina/farmacología , Ratas
2.
Eur J Histochem ; 65(4)2021 Dec 16.
Artículo en Inglés | MEDLINE | ID: mdl-34911286

RESUMEN

The purpose of this work was to prove that oxidative stress is the main mechanism responsible for retinal neurodegenerative changes, subsequent apoptosis, and inflammatory cytokine release in rats fed with a high cholesterol diet (HCD) and determine the role of garlic in alleviating these changes. Forty rats were equally divided into four groups: control, garlic-treated (positive control), HCD, and HCD + garlic-treated (HCD + G). By the end of the experiment (24 weeks) blood samples were collected for assessment of serum lipid profile, oxidative stress parameters, and plasma levels of IL-6 and TNF-α. Both eyes of the rats were enucleated; one was used for light microscopic examination and the other for electron microscopic examination. There was a significant increase in the levels of serum lipids, oxidative stress parameters, IL-6 and TNF-α, and area of expression of caspase-3 in the HCD group compared to both the control and HCD + G groups. Histological examination revealed degenerative changes in all layers of the neural retina in the HCD group. Garlic administration resulted in a significant improvement in the biochemical, immunohistochemical, and histological characteristics of hypercholesterolemic rats. These findings support the hypotheses that garlic has strong antioxidant, anti-apoptotic, and anti-inflammatory properties. Garlic ameliorates the neurodegenerative changes in the neural retina of hypercholesteremic rats.


Asunto(s)
Antiinflamatorios/uso terapéutico , Antioxidantes/uso terapéutico , Enfermedades Neurodegenerativas/tratamiento farmacológico , Extractos Vegetales/uso terapéutico , Retina/efectos de los fármacos , Degeneración Retiniana/tratamiento farmacológico , Animales , Apoptosis/efectos de los fármacos , Citocinas/metabolismo , Dieta Alta en Grasa , Suplementos Dietéticos , Ajo/química , Hipercolesterolemia/complicaciones , Inmunohistoquímica , Masculino , Enfermedades Neurodegenerativas/etiología , Estrés Oxidativo/efectos de los fármacos , Ratas Sprague-Dawley , Retina/patología , Degeneración Retiniana/etiología , Neuronas Retinianas/efectos de los fármacos
3.
Biology (Basel) ; 9(9)2020 Aug 20.
Artículo en Inglés | MEDLINE | ID: mdl-32825436

RESUMEN

BACKGROUND: Sodium valproate (VPA) is an antiepileptic drug (AED) licensed for epilepsy and used during pregnancy in various indications. Alpha-lipoic acid (ALA) is a natural compound inducing endogenous antioxidant production. Our study aimed to investigate the effect of prenatal administration of VPA on the pancreas of rat offspring and assess the potential protective role of ALA co-administration during pregnancy. METHODS: Twenty-eight pregnant female albino rats were divided into four groups: group I (negative control), group II (positive control, ALA treated), group III (VPA-treated), and group IV (VPA-ALA-treated). The pancreases of the rat offspring were removed at the fourth week postpartum and prepared for histological, immune-histochemical, morphometric, molecular, and oxidative stress marker studies. RESULTS: In group III, there were pyknotic nuclei, vacuolated cytoplasm with ballooning of acinar, α, and ß cells of the pancreas. Ultrastructural degeneration of cytoplasmic organelles was detected. Additionally, there was a significant increase in oxidative stress, a decrease in insulin-positive cell percentage, and an increase in glucagon positive cells in comparison to control groups. Moreover, VPA increased the gene expression of an apoptotic marker, caspase-3, with a decrease in anti-apoptotic Bcl2 and nuclear factor erythroid 2-related factor 2 (Nrf2) transcriptional factor. Conversely, ALA improved oxidative stress and apoptosis in group VI, and a consequent improvement of the histological and ultrastructure picture was detected. CONCLUSION: ALA co-administration with VPA significantly improved the oxidative stress condition, histological and morphometric picture of the pancreas, and restored normal expression of related genes, including Nrf2, caspase-3, and Bcl-2. Administration of α-lipoic acid has a protective effect against VPA-induced pancreatic oxidative damage via its cytoprotective antioxidant effect.

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