RESUMO
We retrospectively investigated the natural course of hemoglobin levels after allogenic blood transfusion in total knee arthroplasty. All patients were treated according to the same clinical pathway, and blood tests were performed on the same day. All blood tests were done on pre-op, immediate post-op, midnight of op day, 1st, 2nd, 3rd, 5th, 7th, and 11th day after surgery. Of the total 593 cases, a total of 197 cases (33.2%) were performed within 3 days of surgery. Hemoglobin level was significantly lowest on the 3rd day after surgery and tended to increase afterwards in the non-transfusion group. In the case of blood transfusion on the day of surgery, the hemoglobin level showed an increase on the next day and then showed a minimum value on the fifth day of surgery and then increased. The same pattern was identified when blood transfusion was done on the 1st and 2nd day of surgery. However, when blood transfusion was done on the 3rd day, the hemoglobin level showed a steady increase afterwards. The hemoglobin level of total knee arthroplasty patients with no blood transfusion was the lowest on the 3rd day after surgery and increased afterwards. If blood transfusion was done within 2 days after surgery, the hemoglobin level was the lowest on the 5th day after surgery and increased afterwards. If blood transfusion was done on the 3rd day after surgery, the hemoglobin level increased afterwards.
Assuntos
Artroplastia do Joelho , Transfusão de Sangue Autóloga , Humanos , Estudos Retrospectivos , Perda Sanguínea Cirúrgica , Hemoglobinas/análiseRESUMO
The phytochemical investigation of the roots of Rhus trichocarpa led to this isolation of five new alkyl phloroglucinol derivatives, characterized as (Z)-15-hydroxy-1-(2,4,6-trihydroxyphenyl)-9-octadecen-1-one (named trichocarpol A, 1), (Z)-15-hydroxy-1-(2,6-dihydroxy-4-methoxyphenyl)-9-octadecen-1-one (named trichocarpol B, 2), (Z)-17-hydroxy-1-(2,4,6-trihydroxyphenyl)-9-octadecen-1-one (named trichocarpol C, 3), (Z)-18-hydroxy-1-(2,4,6-trihydroxyphenyl)-9-octadecen-1-one (named trichocarpol D, 4), and (9Z,12Z)-18-hydroxy-1-(2,4,6-trihydroxyphenyl)-9,12-octadecadien-1-one (named trichocarpol E, 5), together with a known compound, 4-(2,6-dihydroxy-4-methoxyphenyl)-4-oxobutanoic acid (6). In vitro cytotoxic activity of compounds 1-6 was evaluated in the human gastric adenocarcinoma AGS cell line and compounds 1-5 showed significant cytotoxicity. Our results indicate that R. trichocarpa, especially the alkyl phloroglucinol derivatives in it, is a good source of promising natural agents for the treatment of gastric cancer.
Assuntos
Adenocarcinoma/tratamento farmacológico , Antineoplásicos Fitogênicos/isolamento & purificação , Floroglucinol/análogos & derivados , Extratos Vegetais/farmacologia , Rhus/química , Neoplasias Gástricas/tratamento farmacológico , Antineoplásicos Fitogênicos/farmacologia , Linhagem Celular Tumoral , Humanos , Espectroscopia de Ressonância Magnética , Estrutura Molecular , Extratos Vegetais/isolamento & purificação , Raízes de Plantas/químicaRESUMO
The neuroprotective potential of flavonoids within the brain comprises anti-apoptosis of neuronal cells, anti-neuroinflammation and enhancement of cognitive function. We reported that Rhus vernciflua inhibits glutamate-induced neurotoxicity in primary cultured rat cortical cells. Here we narrowed it down to get neuroprotective fractions from the plant yielding flavonoid-rich ethyl acetate fraction (PREF). Among its active flavonoids, fisetin exhibited not only inhibitory effect against lipopolysaccharide (LPS)-induced neuroinflammation by suppressing inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 but also memory enhancing effects via reactivation of cAMP responsive element binding protein (CREB)-brain derived neurotrophic factor (BDNF) pathway in memory-impaired mice by scopolamine. Butein also showed a similar activity to fisetin even though to a lesser extent. The neuroprotection by PREF and selected flavonoids may involve maintenance of antioxidant defense mechanism including glutathione peroxidase (GSH-Px), glutathione reductase (GR) and superoxide dismutase (SOD). Conclusively, we demonstrate the R. vernciflua bark extract and its active flavonoids with potent neuroprotective and anti-inflammatory effects might be good therapeutic candidates as cognitive-enhancers.
Assuntos
Anti-Inflamatórios/farmacologia , Cognição/efeitos dos fármacos , Flavonoides/farmacologia , Fármacos Neuroprotetores/farmacologia , Extratos Vegetais/farmacologia , Rhus/química , Animais , Antioxidantes/farmacologia , Cromatografia Líquida de Alta Pressão , Masculino , Camundongos , Camundongos Endogâmicos ICR , Proteínas do Tecido Nervoso/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Casca de Planta/química , Escopolamina/farmacologiaRESUMO
The neuroprotective and anti-inflammatory activities of the methanolic extract of Rhus verniciflua Stokes (Anacardiaceae) were investigated with mouse hippocampal and microglial cells. Bioactivity-guided isolation yielded 10 flavonoids including fustin (1), fisetin (2), sulfuretin (3), butein (4), butin (5), eriodictyol (6), morin hydrate (7), quercetin (8), kaempferol (9) and isoliquiritigenin (10). Among the isolated flavonoids, compounds 2-5 significantly protected the murine hippocampal HT22 cells against glutamate-induced neurotoxicity and attenuated reactive oxygen species (ROS) generations. In addition, these flavonoids significantly maintained antioxidative defense systems preserving the activities of superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GSH-Px) and the content of glutathione (GSH) decreased by glutamate insult. These compounds also showed significant inhibitory effects on LPS-induced nitric oxide (NO) production in BV2 cells. Especially, compound 4 dose-dependently suppressed the expression of both inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). These results suggest that these flavonoids possess therapeutic potentials as a multipotent agent against neurodegenerative diseases related to oxidative stress and pathological inflammatory responses.