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1.
Biomed Res Int ; 2022: 2621732, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35047630

RESUMO

OBJECTIVE: This study is aimed at exploring the effect of ulinastatin combined with Xingnaojing injection on severe traumatic craniocerebral injury and its influence on oxidative stress response and inflammatory response in patients. METHODS: A total of 100 patients with severe traumatic craniocerebral injury admitted to our hospital from January 2018 to January 2020 were selected and equally assigned into a study group (50 cases) and a control group (50 cases) according to a random sampling method. Patients in study group received treatment of ulinastatin combined with Xingnaojing injection, while those in control group were treated with ulinastatin only. The study compared the two groups on the oxidative stress response, inflammatory response, the therapeutic effect, and the incidence rate of adverse reactions. RESULTS: It is observed that patients in study group obtained lower levels of free cortisol (FC) and norepinephrine (NE) in the serum and higher level of total thyroxine (TT4) after treatment compared with those in control group with significant difference (P < 0.05); in the meantime, they were examined to have significantly fewer oxidative stress response products, lower serum inflammatory factor level, and serum indicator levels of craniocerebral injury as opposed to those in control group, suggesting significant differences (P < 0.05); study group demonstrated higher treatment response rate and lower incidence rate of adverse reactions compared with control group with a significant difference (P < 0.05). CONCLUSION: The study found that ulinastatin combined with Xingnaojing infection has a significant effect in the treatment of severe traumatic craniocerebral injury, which can reduce the degree of craniocerebral injury and the level of inflammatory factors in the serum of patients. It is worthy of being promoted and applied clinically.


Assuntos
Traumatismos Craniocerebrais , Medicamentos de Ervas Chinesas/administração & dosagem , Glicoproteínas/administração & dosagem , Estresse Oxidativo/efeitos dos fármacos , Idoso , Traumatismos Craniocerebrais/sangue , Traumatismos Craniocerebrais/tratamento farmacológico , Traumatismos Craniocerebrais/epidemiologia , Feminino , Humanos , Inflamação/sangue , Inflamação/tratamento farmacológico , Inflamação/epidemiologia , Masculino , Pessoa de Meia-Idade
2.
J Stroke Cerebrovasc Dis ; 26(10): 2199-2214, 2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-28645524

RESUMO

BACKGROUND: Orientin has been reported to have extensive pharmaceutical effects of antioxidant, anti-inflammatory, antithrombosis, antiapoptosis, and so on. In the present study, we tried to investigate the protective effects of orientin on cerebral ischemia-reperfusion (I/R) injury and explored the possible mechanisms. METHODS: Middle cerebral artery occlusion rat model was established and then treated with low, middle, and high concentrations of orientin, respectively, with edaravone as a positive control. The treatment effect of orientin was evaluated by measuring the neurological deficit score, cerebral infarction, brain edema, oxidative stress, excitatory amino acids release, the expression levels of aquaporin-4 (AQP-4), and related inflammatory molecules using different methods including immunohistochemistry, enzyme-linked immunosorbent assay, real-time PCR, and western blot. Moreover, morphological and structural changes were also observed by hematoxylin-eosin staining and transmission electron microscope. RESULTS: Orientin provided a significant reduction on neurological deficits, cerebral infarction, cerebral edema, oxidative damage, and neurotoxicity of excitatory amino acids compared to model group (P < .05) in a dose-dependent manner. In addition, orientin substantially downregulated AQP-4 and inflammatory factors expression (P < .05) and improved cell morphology and structure in rats following I/R injury. CONCLUSION: Orientin was able to mediate noticeable protection against cerebral I/R injury through the attenuation of oxidative stress and neurotoxicity of amino acids and inhibiting the upregulation of AQP-4 and inflammatory cytokines.


Assuntos
Isquemia Encefálica/tratamento farmacológico , Isquemia Encefálica/metabolismo , Flavonoides/farmacologia , Glucosídeos/farmacologia , Fármacos Neuroprotetores/farmacologia , Traumatismo por Reperfusão/tratamento farmacológico , Traumatismo por Reperfusão/metabolismo , Animais , Aquaporina 4/metabolismo , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Encéfalo/patologia , Edema Encefálico/tratamento farmacológico , Edema Encefálico/metabolismo , Edema Encefálico/patologia , Isquemia Encefálica/patologia , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Masculino , NF-kappa B/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/fisiologia , RNA Mensageiro/metabolismo , Ratos Sprague-Dawley , Traumatismo por Reperfusão/patologia , Transdução de Sinais/efeitos dos fármacos , Receptor 4 Toll-Like/metabolismo , Fator de Necrose Tumoral alfa/metabolismo
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