RESUMEN
<p><b>Objective</b>To explore the antagonistic effect of vitamin E (VE) on male reproductive toxicity induced by di-2-ethylhexyl phthalate (DEHP) in pubertal SD rats and its underlying mechanisms.</p><p><b>METHODS</b>Thirty 5-week-old male SD rats were randomly divided into five groups of equal number, corn oil control, low-dose (10 mg/kg/d), medium-dose (100 mg/kg/d) and high-dose DEHP exposure (500 mg/kg/d), and VE intervention (high-dose DEHP + VE [100 mg/kg/d]), and treated respectively for 30 successive days. At 3 days after treatment, the testes of the animals were harvested for determination of the oxidative stress index, serum reproductive hormone levels, cauda epididymal sperm parameters, and expressions of cell apoptosis-related genes and proteins.</p><p><b>RESULTS</b>Compared with the control group, the rats of the medium- and high-dose DEHP groups showed significant decreases in the levels of such serum reproductive hormones as follicle-stimulating hormone (FSH), luteinizing hormone (LH) and testosterone (T), sperm parameters as average path velocity (VAP), straight line velocity (VSL), curvilinear velocity (VCL), straightness (STR), linearity (LIN) and wobble (WOB), and the activities of superoxide dismutase (SOD) and glutathione peroxide (GSH-Px), but significant increases were observed in the latter two groups in the content of malondialdehyde (MDA)([3.32±0.87] nmol/mg pro vs [2.13±0.49] nmol/ mg pro), mRNA expressions of Bad, Bax, Cytochrome C, Caspase-3 and the Bax/Bcl-2 ratio, and protein expressions of Cytochrome C and Caspase-3. In comparison with the high-dose DEHP group, the VE intervention group exhibited remarkably increased serum LH and T levels, sperm VAP, VSL, VCL, STR and WOB, and activities of SOD and GSH-Px, but markedly decreased mRNA expressions of Bad, Bax, Cytochrome C, Caspase-3 and the Bax/Bcl-2 ratio as well as the protein expressions of Cytochrome C and Caspase-3 in the testis tissue (P<0.05).</p><p><b>CONCLUSIONS</b>Exposure to DEHP induces androgen secretion disorders, causes oxidative damage to the testicular tissue, activates the mitochondrial apoptosis pathway in the testis, and ultimately reduces the quality of epididymal sperm, while VE can protect the rat testis from DEHP-induced reproductive toxicity.</p>
Asunto(s)
Animales , Masculino , Ratas , Antioxidantes , Farmacología , Apoptosis , Genética , Proteína 5 Relacionada con la Autofagia , Metabolismo , Caspasa 3 , Metabolismo , Dietilhexil Ftalato , Epidídimo , Hormona Folículo Estimulante , Sangre , Hormona Luteinizante , Sangre , Malondialdehído , Metabolismo , Mitocondrias , Estrés Oxidativo , Oxidorreductasas , Metabolismo , Distribución Aleatoria , Ratas Sprague-Dawley , Reproducción , Espermatozoides , Fisiología , Superóxido Dismutasa , Metabolismo , Testículo , Testosterona , Sangre , Vitamina E , FarmacologíaRESUMEN
This study is to investigate protective effect of safflor yellow B (SYB) against vascular endothelial cells (VECs) injury induced by angiotensin-II (Ang-II). VECs were cultured and divided into six groups: control group, Ang-II group, Ang-II + SYB (1 micromolL(-1)) group, Ang-II + SYB (10 micromolL(-1)) group, Ang-II + SYB (100 micromolL(-1)) group and Ang- II + verapamil (10 micromolL(-1)) group. Except control group, all of VECs in other groups were treated with Ang- II at the final concentration of 0.1 micromolL(-1). Mitochondria membrane potential (MMP) and free calcium concentration ([Ca2+]i) were measured by laser scanning confocal microscopy, and mitochondria complex IV activity was detected by BCA method. The levels of reactive oxygen species (ROS) in VECs were analyzed by fluorescence detector and apoptosis of VECs was observed by flow cytometer. Caspase 3 was determined by Western blotting method. Comparing with control group, Ang-II was able to increase [Ca2+]i and ROS level, decrease MMP level, inhibit complex IV activity and enhance caspase 3 activity in VECs, as a result, enhance apoptosis of VECs. But SYB could significantly reduce the result induced by Ang- II relying on different dosages (P < 0.05 or P < 0.01). SYB was able to eliminate the effect of Ang-II on VECs via regulating [Ca2+]i, mitochondrial structure and function and inhibiting apoptosis.
Asunto(s)
Humanos , Angiotensina II , Antioxidantes , Farmacología , Apoptosis , Calcio , Metabolismo , Carthamus tinctorius , Química , Caspasa 3 , Metabolismo , Células Cultivadas , Chalcona , Farmacología , Medicamentos Herbarios Chinos , Farmacología , Complejo IV de Transporte de Electrones , Metabolismo , Células Endoteliales , Biología Celular , Metabolismo , Potencial de la Membrana Mitocondrial , ATPasas de Translocación de Protón Mitocondriales , Metabolismo , Plantas Medicinales , Química , Especies Reactivas de Oxígeno , Metabolismo , VasoconstrictoresRESUMEN
<p><b>OBJECTIVE</b>To study the protective effect of ligusticum chuanxiong phthalides on cerebral ischemia in rats and its related mechanism of action.</p><p><b>METHOD</b>Middle cerebral artery occlusion (MCAO) model, thrombosis formation, platelet aggregation and hemorrheological parameters were measured to evaluate the protective effect of ligusticum chuanxiong phthalides.</p><p><b>RESULT</b>Ligusticum chuanxiong phthalides could markedly decrease the infarct size and behavior deficits score, inhibit the thrombus formation and platelet aggregation, ameliorate hemorrheological parameters with a dose-dependent manner in rats.</p><p><b>CONCLUSION</b>Ligusticum chuanxiong phthalides has protective effects on focal cerebral ischemia in rats, and its mechanism may be relevant to its inhibition of platelet-dependent thrombosis and amelioration of hemorrheological parameters.</p>