RESUMEN
In this study, Black chokeberry (Aronia melanocarpa) was used as an example to provide reference for improving the safety, efficacy and quality consistency of homologous foods. In this study, two quality markers (Q-markers) of 27 batches of Black chokeberry were determined using high performance liquid chromatography (HPLC), and there were some differences among the 27 samples. Origin B samples had the highest levels of Q-markers for S15, and origin C had lower than average levels overall. Samples were analyzed qualitatively and quantitatively by Systematic Quantitative Fingerprinting (SQFM). Subsequently, a three-wavelength fusion analysis (TWFP) was established on the chromatographic data to compensate for the lack of a single wavelength. Fourteen batches of TWFP samples were rated at Level 5 or above in the SQFM assessment, indicating that there is some variation in the content of samples from different origins. Principal component analysis (PCA) was used to observe the differences in chemical composition and content of TWFP samples. Subsequently, electrochemical fingerprinting (ECFP) was established and nine characteristic parameters were recorded, showing that the samples were suppressed for all electrochemical Belousov-Zhabotinsky oscillation systems (B-Z oscillation systems). Finally, antioxidant tests were performed using DPPH. The antioxidant capacity was predicted using Partial Least Squares (PLS) analysis with R2Y = 0.84, Q2 = 0.77, a good model fit and accurate prediction. The fingerprint-potency relationship between IC50-peak area showed that 17 of the 19 shared peaks were negatively correlated, indicating that 17 peaks contributed significantly to the antioxidant. The methods established in this study for the determination of TWFP and ECFP, as well as the spectral relationships with peak area and IC50, can be used for the quality inspection and antioxidant capacity test of Black chokeberry, which provides a new research direction for improving the quality standard of medicinal and foodstuffs.
Asunto(s)
Antioxidantes , Frutas , Photinia , Control de Calidad , Photinia/química , Antioxidantes/química , Antioxidantes/análisis , Cromatografía Líquida de Alta Presión , Frutas/química , Técnicas Electroquímicas , Extractos Vegetales/química , Análisis de Componente PrincipalRESUMEN
BACKGROUND: High-intensity exercise consumes a large amount of energy and tends to induce post-exercise fatigue. Promoting physical and psychological recovery after exercise can enable individuals to perform better in subsequent training or competitions and reduce the risk of injury. This study aims to investigate the effects of post-exercise recovery methods on exercise-induced hormones and blood fatigue factors. METHODS: PubMed, Embase and Web of Science databases were queried to collect literature on the correlation between post-exercise recovery methods and the expression of exercise-induced hormones and blood fatigue factors. The search time ranged between inception to July 2020. Stata (version 15.0) was used for meta-analysis. RESULTS: A total of 10 studies were included, involving the data of 278 cases. Among these, 148 people were placed in the study group and assigned active post-exercise recovery measures while 130 people were placed in the control group and assigned no post-exercise recovery measures. The results of this meta-analysis showed that there was significant difference between the study group and the control group [relative risk (RR) =15.62, 95% confidence interval (CI): 3.25, 75.06, P<0.05]. The subgroup analysis on the effect of active and passive recovery on the blood lactate concentration (BLC) and creatine kinase (CK) concentration revealed that the CK concentration [standardized mean difference (SMD) =-0.76, 95% CI: -1.47, -0.04] and BLC (SMD =-1.16, 95% CI: -2.30, -0.02) were significantly lower in the study group compared with the control group. Further analysis on the effect of different post-exercise recovery methods on the BLC and CK concentrations indicated that BLC (SMD =-1.16, 95% CI: -2.30, -0.02) was significantly lower in the group with cold water immersion compared with the control group, while there was no significant difference in the changes of CK concentration. Additionally, food supplementation was shown to reduce CK concentration (SMD =-1.16, 95% CI: -4.69, 2.36). CONCLUSIONS: Recovery measures after high-intensity exercise can accelerate the reduction of BLC and the activity and concentration of CK, thus helping the body quickly return to a pre-exercise state.
Asunto(s)
Ejercicio Físico , Fatiga , Hormonas , HumanosRESUMEN
Vinpocetine is an inhibitor of phosphodiesterase type 1 (PDE1), which has been used for treating stroke for over 40 years. However, according to current clinical dosage and treatment period, its direct effect on memory is unclear. In this study, we investigated whether vinpocetine could reverse the scopolamine (SCO)-induced cognitive deficits in animals. Behavioral experiments, including open field, Y-maze, and fear conditioning tests were used to determine the possible role of vinpocetine on scopolamine-induced memory dysfunction. In the open field and Y-maze tests, there were significant differences between the control (CON) group and SCO group. Vinpocetine (4 mg/kg) administration for consecutive 28 d significantly improved the scopolamine-induced memory dysfunction. In the fear conditioning test, vinpocetine (2, 4 mg/kg) administration had certain beneficial effect on emotional memory. Our results suggest that vinpocetine could improve cognitive function in memory deficient mice and high clinic dosage might be better.
Asunto(s)
Demencia/tratamiento farmacológico , Trastornos de la Memoria/tratamiento farmacológico , Fármacos Neuroprotectores/uso terapéutico , Alcaloides de la Vinca/uso terapéutico , Animales , Reacción de Prevención/efectos de los fármacos , Conducta Animal/efectos de los fármacos , Condicionamiento Psicológico/efectos de los fármacos , Demencia/inducido químicamente , Miedo , Locomoción/efectos de los fármacos , Masculino , Aprendizaje por Laberinto/efectos de los fármacos , Trastornos de la Memoria/inducido químicamente , Ratones Endogámicos C57BL , EscopolaminaRESUMEN
OBJECTIVE: To observe the effects of dexmedetomidine (DEX) on glutamate (Glu), aspartic acid (Asp) release and NMDAR1 expression in hippocampus in global cerebral ischemia/reperfusion rats, and investigate the protective effect and the related mechanism of neurotransmitters. METHODS: Fifty-four male Wistar rats were randomly divided into three groups (n=18):sham group(A), ischemia/reperfusion group(B), dexmedetomidine pretreatment group(C). Total cerebral ischemia model was set up by four vessel occlusion in rats. Glu and Asp levels were measured with microdialysis at different time. Then the animals were decapitated and the brains were immediately removed to detect NMDAR1 expression in hippocampus area by immunohistochemistry and Western-blot. RESULTS: Compared with that in group B, the levels of Glu, Asp and NMDA NR1 protein were significantly decreased in the dexmedetomidine pretreatment group (P<0.05 or 0.01). CONCLUSIONS: Dexmedetomidine might has a protective effect on hippocampus in global cerebral ischemia/reperfusion animals. The protective mechanism might be involved in inhibiting excitatory amino acids(EAA) release and NMDAR1 expression.
Asunto(s)
Isquemia Encefálica/metabolismo , Dexmedetomidina/farmacología , Aminoácidos Excitadores/metabolismo , Hipocampo/efectos de los fármacos , Receptores de N-Metil-D-Aspartato/metabolismo , Daño por Reperfusión , Animales , Masculino , Ratas , Ratas Sprague-Dawley , Ratas WistarRESUMEN
OBJECTIVE: To investigate the effect of penehyclidine hydrochloride on glutamate (Glu)release and N-methyl-D-aspartate receptor (NMDAR)1 expression in hippocampus CA1 with global cerebral ischemia/reperfusion rats. METHODS: Sixty male Wistar rats were randomly allocated into three groups; group A received sham operation; group B received ischemia/reperfusion; group C received penehyclidine hydrochloride treatment (2 mg/kg) before ischemia/reperfusion (n=20). Global cerebral ischemia was induced according to Pulsinelli-Brierley method. All animals were divided into two experiments: (I) Microdialysis plus HPLC/FD were used to detect Glu level after reperfusion 1 h, 3 h, 6 h. (II) After reperfusion 3 h, the animals were decapitated on ice and the brains were immediately removed to detect NMDAR1 expression in CA1 area by immunohistochemistry. RESULTS: After penehyclidine hydrochloride treatment, extracellular Glu level in CA1 were significantly decreased compared with those of control group (P < 0.05 or 0.01); Total integrated OD, average gray value and positive-cell area of NMDAR1 in CA1 were also significantly decreased compared with those of control group (P < 0.05 or 0.01). CONCLUSION: Penehyclidine hydrochloride might has protective effect in hippocampus CA1 on global cerebral ischemia/reperfusion animals. The protective mechanism might be involved in inhibiting Glu release and NMDAR1 expression.
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Isquemia Encefálica/fisiopatología , Ácido Glutámico/metabolismo , Quinuclidinas/farmacología , Receptores de N-Metil-D-Aspartato/metabolismo , Daño por Reperfusión/prevención & control , Animales , Isquemia Encefálica/metabolismo , Región CA1 Hipocampal/metabolismo , Antagonistas Colinérgicos/farmacología , Masculino , Ratas , Ratas Sprague-Dawley , Daño por Reperfusión/metabolismoAsunto(s)
Giro Dentado/metabolismo , Epilepsia/metabolismo , Proteína Ácida Fibrilar de la Glía/metabolismo , Hipocampo/metabolismo , Proteínas Asociadas a Microtúbulos/metabolismo , Neuropéptidos/metabolismo , Animales , Proteínas de Dominio Doblecortina , Proteína Doblecortina , Epilepsia/inducido químicamente , Ácido Kaínico , Masculino , Ratones , Ratones Endogámicos C57BL , Neuronas/metabolismoRESUMEN
To investigate the analgesic effect of intrathecally administered γ-aminobutyric acid (GABA) transporter-1 inhibitor NO-711 on the sciatic nerve chronic constriction injury (CCI) rats. 5 days after intrathecal catheter placement, neuropathic pain model was established by CCI of sciatic nerve on rats. Withdrawal thresholds for mechanical allodynia and latency for thermal hyperalgesia were measured in all animals. All rats operated upon for CCI displayed decreased withdrawal thresholds for mechanical allodynia and latency for thermal hyperalgesia, which has significant difference compared with sham groups. After intrathecal NO-711 administration, withdrawal thresholds and latency were significantly increased on CCI rats compared with control group after 1 day. The results show that GABA transporter-1 inhibitor could effectively develop analgesic effect in sciatic nerve CCI rats' model.
Asunto(s)
Antagonistas del GABA/uso terapéutico , Hiperalgesia/tratamiento farmacológico , Neuralgia/tratamiento farmacológico , Inhibidores de la Captación de Neurotransmisores/uso terapéutico , Ácidos Nipecóticos/uso terapéutico , Oximas/uso terapéutico , Dimensión del Dolor/efectos de los fármacos , Umbral del Dolor/efectos de los fármacos , Animales , Antagonistas del GABA/farmacología , Calor , Inyecciones Espinales , Masculino , Inhibidores de la Captación de Neurotransmisores/farmacología , Ácidos Nipecóticos/farmacología , Oximas/farmacología , Estimulación Física , Distribución Aleatoria , Ratas , Ratas Sprague-Dawley , Nervio Ciático/lesiones , Neuropatía Ciática/tratamiento farmacológicoRESUMEN
Long-term neuroplastic changes in dentate gyrus (DG) have been reported after seizure induction and were shown to contribute to epitogenesis of epilepsy. These changes include increased number of newborn granule cells, sprouted mossy fibers, granule cell layer dispersion, etc. The aim of current study is to determine the acute progression of neuroplastic changes involved newly generated granule cells after kainic acid (KA)-induced seizures. Doublecortion (DCX) analysis was used to examine the newly generated granule cells morphology 1-7 days after seizure induction. Quantitative analysis of DCX-labeled cells at different times shows that there are some rapid changes in the dentate gyrus. At day 7 epileptical mice induced an increase of the number of DCX-labeled cells in DG. At days 3 and 7 after epilepsy induction, the percentage of DCX-labeled cells per DG were significantly increased. These results show that seizures are capable to increase the number of new granule cell within a short time for function activation in post-seizure period. Therefore, the rapid changes in the DG might be having a potential for hippocampus neuroplastic function.
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Giro Dentado/patología , Hipocampo/patología , Plasticidad Neuronal , Convulsiones/patología , Animales , Anticuerpos , Giro Dentado/citología , Giro Dentado/fisiología , Modelos Animales de Enfermedad , Proteínas de Dominio Doblecortina , Proteína Doblecortina , Hipocampo/fisiología , Ácido Kaínico , Ratones , Ratones Endogámicos C57BL , Proteínas Asociadas a Microtúbulos/inmunología , Neuropéptidos/inmunología , Convulsiones/inducido químicamente , Coloración y Etiquetado , Factores de TiempoAsunto(s)
Isquemia Encefálica/metabolismo , Proteína Ácida Fibrilar de la Glía/metabolismo , Fármacos Neuroprotectores/farmacología , Propofol/farmacología , Daño por Reperfusión/prevención & control , Animales , Astrocitos/metabolismo , Isquemia Encefálica/patología , Distribución Aleatoria , Ratas , Ratas Wistar , Daño por Reperfusión/metabolismoRESUMEN
AIM: To observe the change of STR neuronal firing rates with high frequency stimulation of subthalamic nucleus in PD rats. METHODS: A model of Parkinson's disease was induced by unilateral administration of 6-hydroxydopamine into right substantia nigra in rats. After the high-frequency stimulation to STN, the spontaneous firing rates of STR on normal and PD rats were recorded by using extracellular recordings. RESULTS: Stimulation caused a direct excited effect of STR neurons in normal rats whereas a excited and inhibited effect in PD rats. The inhibited effect was correlated with the stimulation period (r = 0.94). CONCLUSION: Stimulation to STN may inhibit the spontaneous firing rates of STR neurons in PD rats. These results also give some clues that high-frequency stimulation to STN may be a effective therapy to the clinical treatment of Parkinson's disease.