Effects of urotensin II (UII) on paraventricular nucleus (PVN) neurons of hypothalamus from brain slices of rats were examined by using extracellular recording technique. The results are as follows: (1) In response to application of UII (0.3, 3.0, 30.0, 300.0 nmol/L, n=39) into the perfusate for 2 min, the spontaneous discharge rates (SDR) of 32/39 (82.05% ) neurons were significantly decreased in a dose-dependent manner; (2) Pretreatment with bicuculline (BIC, 100 μmol/L), a specific GABAA receptor antagonist, led to a marked increase in SDR of 5/7 ( 71.43% ) neurons in an epileptiform pattern. The increased discharges were not significantly changed after UII ( 30.0 nmol/L ) was applied into the perfusate for 2 min; (3) Pretreatment with picrotoxin ( PIC, 50 μmol/L ), a selective blocker of Cl- channel, led to an increase in the SDR of all 12/12 (100%) neurons. The increased discharges were not influenced by the applied UII (30.0 nmol/L) for 2 min in 11/12 (91.67%) neurons; (4) Application of nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 50 μmol/L ) into the perfusate could significantly augment the SDR of 11/12 ( 91.67% ) neurons , while UII ( 30.0 nmol/L ) applied into the perfusate for 2 min led the augmented SDR of all (12/12, 100%) neurons decrease. The results suggest that UII decreases the excitability of PVN neurons of hypothalamus by potentiating GABAA receptor-mediated Cl- current.

AIM To study the central role of genistein (GST) in regulating cardiovascular function of nervous center by examining the effects of GST on the electrical activity of rat paraventricular nucleus neurons in slice preparation and to elucidate the mechanism involved. METHODS Using extracellular single-unit discharge recording technique to examine discharges of neurons in paraventricular nucleus of hypothalamic slices at the resting potential level. RESULTS ①In response to the application of GST 10, 50 and 100 μmol·L-1, respectively, in the perfusate for 2 min, the spontaneous discharge rates (SDR) of neurons in 25/26 hypothalamic slices were significantly decreased in a concentration-dependent manner. ②Pretreatment with L-glutamate 0.2 mmol·L-1 led to a marked increase in the SDR of slices in an epileptiform pattern. GST 50 μmol·L-1 significantly attenuated the increased SDR in all 7 slices. ③In 8/8 slices, the G protein-coupled inwardly rectifying K+ channels (GIRKs) antagonist, tetraethylammonium 1 mmol·L-1 completely blocked the inhibitory effect of GST 50 μmol·L-1. ④Pretreatment with nitric oxide synthase inhibitor Nω-nitro-L-arginine methyl ester 50 μmol·L-1 increased SDR in all 7 slices, but did not affect the inhibitory effect of GST 50 μmol·L-1. CONCLUSION GST can inhibit the electrical activity of paraventricular neurons, and play a protective role on the central neurons. The inhibitory effect of GST may be related to the activation of GIRKs which induce K+ outward current and then engender the cell membrane hyperpolarization, but be not due to the NO release.

Extracellular single-unit discharge recording technique was used to examine the effects of Ginkgolide B (BN52021) on the discharges of neurons in CAI area of hippocampal slices and to elucidate the mechanisms involved.The results showed that:(1) In response to the application of ginkgolide B (0.1,1,10 βμmol/L; n =43) into the perfusate for 2 rain,the spontaneous discharge rates (SDR) of 42/43 (97.67%) neurons were significantly decreased in a dose-dependent manner; (2) Pretreatment with L-glutamate (L-Glu,0.2mmol/L) led to a marked increase in the SDR of all 10 (100%) neurons in an epileptiform pattern.The increased discharges were suppressed significantly after ginkgolide B (1 μmol/L) was applied into the perfusate for 2 rain; (3) In 8 neurons,perfusion of the selective L-type calcium channel agonist,Bay K 8644 (0.1 μmol/L),induced a significant increase in the discharge rate of 8/8 (100%) neurons.Ginkgolide B (1 μmoL/L) applied into the perfusate inhibited the discharges of 7/8 (87.5%) slices; (4) In 8 neurons,the broad potassium channels blocker,tetraethylammonium (TEA,1 mmol/L) completely blocked the inhibitory effect of ginkgolide B (1 μmol/L).These results suggest that ginkgolide B can inhibit the electrical activity of CAI neurons.The inhibitory effect may be related to the blockade of L-type voltage-activated calcium channel and may be concerned with delayed rectifier potassium channel (KDR),which indicated that ginkgolide B play a protective role on the central neurons.

BACKGROUND:Acute exercise is believed to regulate appetite and influence feeding behaviors by controling the synthesis and secretion of gastrointestinal peptide hormones to regulate appetite and feeding behavior influence, but the smal sample size leads to widely different results.
OBJECTIVE:To clarify the effect of acute exercise on peptide YY levels in adults using Meta-analysis method. METHODS:A computer-based search of PubMed, Google Scholar, Sport Discus, Web of Knowledge and CNKI was performed for relevant articles published before January 2014. The literatures eligible were studied by evaluating the publication bias, checking the heterogeneity and analyzing the sensitivity by software of RevMan5.1.
RESULTS AND CONCLUSION:(1) There were a total of 188 participants in the 18 trials reported in 11 articles. The Meta-analysis results revealed a mean effect for acute exercise to increase peptide YY values (standardized mean difference=0.25, 95% confidence interval =0.05-0.46,P=0.01), and therefore, there was a significantly statistical difference in the peptide YY levels between the acute exercise group and control group (P< 0.05). Moreover, results from the sensitivity analysis showed no influences on the findings of Meta-analysis. (2) Five randomized controled trails in the three included articles were related to peptide YY (3-36). There was a maximal heterogeneity among these studies; therefore, a random-effect model was utilized. The result revealed a mean effect for acute exercise to increase peptide YY (3-36) values (standardized mean difference =1.80, 95% confidence interval =0.27-3.32,P=0.02). The findings from this meta-analysis show that acute exercise may influence appetite by increasing levels of peptide YY in adults.

Though parched Chinese herbal medicines contain less effective or index components, their pharmacological actions do not reduce or even become improved to some extent. However, the current studies related to material basis could not explain the changes in property, flavour and efficacy of parched Chinese herbal medicines. Meanwhile, due to the lack of objective and specific evaluation indexes, the quality evaluation could not reflect features of parched Chinese herbal pieces. Therefore, how to break the bottleneck for the studies on parched Chinese herbal pieces, make further innovation and conduct in-depth studies on the material basis of parched Chinese herbal medicines are common problems that medical scholars are facing. According to the findings in the previous studies, the author proposed to explain the material basis of parched Chinese herbal medicines by studying Maillard reaction and establish specific quality evaluation indexes according to the features of parched Chinese herbal pieces, and conducted relevant studies.
Drug Compounding ; methods ; Drugs, Chinese Herbal ; chemistry ; Maillard Reaction ; Quality Control

Humans ; Large-Conductance Calcium-Activated Potassium Channels ; TRPC Cation Channels ; Vasodilation

BACKGROUND:A large number of clinical trials have found that the number of bone marrow stem cels at the femoral neck and proximal femur in patients with osteonecrosis of the femoral head is significantly reduced, accompanied by decreased activity, which causes a significant decrease in osteogenic capacity that the necrotic bone cannot be effectively repaired after absorption, leading to the colapse of the femoral head. OBJECTIVE:To probe into the early clinical efficacy of autologous peripheral blood mononuclear cel transplantation with porous core decompression for treatment of avascular necrosis of the femoral head. METHODS:Forty-five patients with avascular necrosis of the femoral head (49 hips) were enroled in this study, and underwent autologous peripheral blood mononuclear cel transplantation with porous core decompression. After treatment, pain scores, Harris hip score, scores on the satisfaction of patients were evaluated, as wel as X-ray, CT and MRI examinations. RESULTS AND CONCLUSION:Al the patients received a folow-up visit of 11-14 months, averagely (12.5±0.6) months. During the folow-up, there were no complications and serious adverse reactions. Postoperative pain scores and Harris scores were both improved significantly compared with preoperative ones (P < 0.05). At 12 months after treatment, the excelent satisfaction rate was up to 92%. Patient’s MRI low signal region accounting for a percentage of the volume of the femoral head was decreased from (40.1±7.34)% preoperatively to (20.23±5.4)% at 6 months postoperatively, and there was a significant difference (P < 0.05). These findings indicate that autologous peripheral blood mononuclear cel transplantation with porous core decompression for treatment of avascular necrosis of the femoral head has significantly clinical effects at early stage, which can obviously reduce joint pain, improve and restore hip joint function, and delay progression of disease.

Objective To study interleukin-1 receptor(IL-1R) and connexin(Cx36) gene expression following Mg 2+-free-induced seizures in cultured developing neuron. Methods Rat embryo cortical neurons cultured for 6 and 17 days were exposed to Mg 2+-free media to induce seizure. At different time after Mg 2+-free treatment, real-time RT-PCR was used to detect IL-1R and Cx36 mRNA expression. Results 1. IL-1R mRNA expression transiently decreased after Mg 2+-free treatment in neurons cultured for 6 and 17 days in vitro. Then the levels of IL-1R mRNA expression recovered in neurons cultured for 6 days, but IL-1R mRNA expression were increased in neurons cultured for 17 days compared with control group and the peak was at 24 hours. 2. In neurons cultured for 6 days in vitro, Cx36 mRNA expression increased after Mg 2+-free treatment compared with control group, the peak was at 24 hours. But in neurons cultured for 17 days in vitro, Cx36 mRNA expression decreased at 6 hours after Mg 2+-free treatment compared with control group, the peak was at 24 hours. Conclusions IL-1R mRNA and Cx36 mRNA expression following Mg 2+-free-induced seizures are different between the neurons cultured for 6 and 17 days in vitro. This is possibly related to the different neuron injury between 6 and 17 days in vitro following seizures.

This study is to evaluate the effect of resveratrol on carotid baroreceptor activity (CBA). The functional curve of carotid baroreceptor (FCCB) was constructed and the functional parameters of carotid baroreceptor were measured by recording sinus nerve afferent discharge in anesthetized male rats with perfused isolated carotid sinus. Resveratrol (30, 60 and 120 μmol·L-1) inhibited CBA, which shifted FCCB to the right and downward. There was a marked decrease in peak slope (PS) and peak integral value (PIV) of carotid sinus nerve charge in a concentration-dependent manner. Pretreatment with Nω-nitro-L-arginine methyl ester (L-NAME, 100 μmol·L-1), an inhibitor of nitric oxide synthase (NOS), eliminated the inhibitory effect of resveratrol. Pretreatment with Bay K8644 (an agonist of L-type calcium channel, 500 nmol·L-1) abolished the effect of resveratrol on CBA. A potent inhibitor of tyrosine phosphatase (sodium orthovanadate, 1 mmol·L-1) did not influence the effect of resveratrol on CBA. Resveratrol inhibits carotid baroreceptor activity, which may be mediated by the locally released NO and decreased calcium influx. Several studies have showed a cardioprotective effect of resveratrol, with the penetrating study of resveratrol, it may show a potential value in the clinical treatment of cardiovascular disease as an alternative medicine.

AIM To study the relationship between cardioprotective effects of resveratrol and carotid sinus baroreflex (CSB). METHODS The functional curve of the CSB was measured by recording changes in arterial pressure in anesthetized male rats with perfused isolated carotid sinus. RESULTS Resveratrol (30, 60 and 120 μmol·L-1) inhibited the CSB, which shifted the functional curve of the baroreflex to the right and upward. There were a marked decrease in peak slope and a reflex decrease of blood pressure, and also an increase in threshold pressure. Changes of these parameters showed a concentration-dependent manner. Pretreatment with Nω-nitro-L-arginine methylester (100 μmol·L-1), an inhibitor of nitric oxide synthase, and pretreatment with Bay K8644 (500 nmol·L-1), an agonist of L-type calcium channel, could both eliminate the inhibitory effect of resveratrol on CSB. A potent inhibitor of tyrosine phosphatase sodium orthovanadate (1 mmol·L-1) did not influence the effect of resveratrol on CSB. CONCLUSION Resveratrol inhibits carotid baroreflex, which may be mediated by the locally released NO and decreased calcium influx.