Objective:To optimize the extraction process of Guilong cataplasm .Methods:The yield of volatile oil was used as the index to optimize the volatile oil extraction technology by single factor tests. The yield of dry extract and the content of aconitine were used as the indices to optimize the water extraction technology by single factor tests and orthogonal test .Results:The optimal extraction conditions of volatile oil were as follows:the soaking time was 1h with 8-fold volume of water , and the extraction time was 6 hours.The optimal water extraction conditions were as follows:using 8-fold volume of water extracted for 3 times with 1 h for each time .Conclu-sion:The extraction process is simple , reasonable and reproducible ,which is suitable for the next research of Guilong cataplasm .

Objective: To observe the effects of swimming plus medication on the expressions of cytokines in rats with chronic abacterial prostatitis (CAP). METHODS: Forty healthy adult male SD rats were randomly divided into five groups of equal number, normal control, CAP model control, medication, exercise therapy, and exercise + medication. The CAP model was made by Xiaozhiling injection, and at 7 days after modeling, the rats in the medication and exercise + medication groups were treated intragastrically with Qianlie Shutong Capsules (0.016 g/ml) at 20 ml per kg of the body weight qd, those in the exercise therapy and exercise + medication groups were made swim at a regular time once a day, 35 minutes on the first day and 5 minutes more on the second until 50 minutes once, for 4 successive weeks, and those in the normal control, model control and exercise therapy groups received normal saline only. After 14 and 28 days of treatment, all the rats were killed and their prostates harvested for observation of histopathological changes and determination of the expressions of TNF- α, IL-1β and IL-6 in the prostatic tissue homogenate by ELISA. RESULTS: After 14 days of treatment, the expression levels of TNF-α, IL-1β and IL-6 were significantly elevated in the groups of CAP model control (［183.08±8.07］ pg/ml, ［57.55±3.53］ pg/ml and ［256.15±13.95］ ng/L), medication (［118.49±8.06］ pg/ml, ［42.64±4.64 ］ pg/ml and ［200.74±9.33］ ng/L), exercise therapy (［169.63±10.64］ pg/ml, ［50.45±5.71］ pg/ml and ［245.23±6.49］ ng/L), and exercise + medication (［107.82±7.81］ pg/ml, ［40.35±6.93］ pg/ml and ［187.04±10.85］ ng/L) as compared with those in the normal control (［20.36±1.82］ pg/ml, ［14.64±1.91］ pg/ml and ［70.58±2.09］ ng/L) (P<0.05). At 28 days, the levels of TNF- α, IL-1β, IL-6 were remarkably lower in the exercise + medication group (［29.30±3.78］ pg/ml, ［16.91±1.24］ pg/ml and ［ 88.65±6.74］ ng/L) than in the medication group (［39.67±3.19］ pg/ml, ［26.27±3.49］ pg/ml and ［110.26±6.33］ ng/L) (P<0.05) and close to those of the normal control group (［19.34±1.76］ pg/ml, ［13.68±1.06］ pg/ml and ［71.34±2.50］ ng/L). During the treatment, no obvious pathological changes were found in the prostate tissue of the normal control rats, while significant chronic prostatic inflammation was observed in the CAP models, and the inflammation was relieved in different degrees after intervention, most significantly in the exercise + medication group. CONCLUSIONS Swimming can relieve prostatic inflammation and swimming plus medication can effectively reduce the expressions of cytokines and alleviate histological damage in the prostatic tissue of CAP rats.
Animals ; Chronic Disease ; Combined Modality Therapy ; methods ; Cytokines ; metabolism ; Drugs, Chinese Herbal ; therapeutic use ; Interleukin-1beta ; metabolism ; Interleukin-6 ; metabolism ; Male ; Physical Conditioning, Animal ; Prostatitis ; metabolism ; therapy ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Swimming ; Time Factors ; Tumor Necrosis Factor-alpha ; metabolism

Adolescent ; Adult ; Aged ; Antithyroid Agents ; administration & dosage ; adverse effects ; therapeutic use ; Biomarkers ; blood ; Female ; Hepatitis B ; complications ; pathology ; Hepatitis, Viral, Human ; complications ; pathology ; Humans ; Hyperthyroidism ; complications ; drug therapy ; Liver Function Tests ; Male ; Methimazole ; administration & dosage ; adverse effects ; therapeutic use ; Middle Aged ; Propylthiouracil ; administration & dosage ; adverse effects ; therapeutic use ; Retrospective Studies ; Severity of Illness Index ; Thyroid Function Tests ; Young Adult

Objective: To evaluate the role of hippocampal neuronal nitric oxide synthase (nNOS)-postsynaptic dense protein 95 (PSD95) coupling in short-term memory retrieval disorder induced by sevoflurane in mice. Methods: Sixteen clean-grade healthy Kunming mice of both sexes, aged 2-3 months, weighing 30-35 g, were divided into 2 groups (n=8 each) according to the random number table method: sevoflurane group (S group) and nNOS-PSD95 uncoupling agent ZL006 group (Z group). After successful establishment of dark avoidance memory, 3.3% sevoflurane and 40% O₂ were inhaled for 2 h in both groups, and normal saline 1.5 ml was intraperitoneally injected in group S and ZL006 1 mg/kg in group Z at 30 min before anesthesia.The step-through latency and error times were recorded before anesthesia and at 12 h after the end of anesthesia.The mice were then sacrificed, and hippocampal tissues were taken for determination of the expression of nNOS and PSD95 (by Western blot) and co-expression of nNOS and PSD95 (by immunoprecipitation). Results: Compared with that before anesthesia, the step-through latency was significantly shortened, and the error times were increased at 12 h after anesthesia in group S (P<0.05), and no significant change was found in the above indicators in group Z (P>0.05). Compared with group S, the step-through latency was significantly prolonged, error times were decreased, the co-expression of nNOS and PSD95 was down-regulated (P<0.05), and no significant change was found in the expression of nNOS and PSD95 in group Z (P>0.05). Conclusion The mechanism by which sevoflurane induces short-term memory retrieval disorder may be related to promoting the coupling of nNOS to PSD95 in the hippocampus of mice.

To observe the effects of hypothermia on the repolarization duration and the expression of Kir2.1 protein of ventricular myocytes in isolated rat heart and explore the role of Kir2.1 protein. Eighteen healthy adult male Sprague-Dawley rats were randomly divided into three groups (n=6 per group): Control group (C group), 35℃ group (H group), 32℃ group (H group). Langendorff isolated heart models were established. After 15 min 37℃ K-H fluid banlanced perfusion, C group continued to perfuse the K-H solution at 37℃ for 30 minutes, H group continued to perfuse the K-H solution at 35℃ for 30 minutes, H group continued to perfuse the K-H solution at 32℃ for 30 minutes. At 15 min of balanced perfusion (T), and 30 min of continuous perfusion (T), the heart rate,and the MAP in the three layers of the left ventricular anterior wall were recorded, the action potential duration at 50% repolarization (MAPD), the action potential duration at 90% repolarization (MAPD) and transmural dispersion of repolarization(TDR) were calculated. At the same time, the occurrence of arrhythmia was recorded. The expression of Kir2.1 protein was measured by Western blot. The average optical density (AOD) and the distribution of Kir2.1 protein were measured by immunohistochemistry in the ventricular tissue measured by electrophysiology. Compared with T, the heart rate was decreased, MAPD and MAPD were prolonged significantly (P＜0.05), and TDR was increased significantly (P＜0.05) in H group, H group at T. Compared with C group, the HR was decreased, the MAPD was prolonged significantly (P＜0.05), TDR was increased significantly (P＜0.05),the expression and the AOD of Kir2.1 protein were decreased significantly (P＜0.05) in Hgroup, Hgroup at T. Compared with H group, the heart rate of H group was decreased significantly (P＜0.05), MAPD and MAPD were prolonged significantly (P＜0.05), and TDR was increased significantly (P＜0.05) at T. The distribution of Kir2.1 protein in group C was normal, while the distribution of Kir2.1 in H group and H group was disordered. Hypothermia prolonged the ventricular duration of repolarization and increased the dispersion of repolarization. The mechanism is related to the down-regulation the expression of Kir2.1 protein and the disorder of the distribution of Kir2.1 protein.

Objective: To evaluate the effect of sevoflurane on phosphorylation of connexin 43 (Cx43) at Ser368 (Cx43 Ser368) in ventricular myocardium in isolated hearts of diabetic rats. Methods: Twenty-four clean-grade healthy adult male Sprague-Dawley rats, aged 3 months, weighing 180-220 g, were used in this study.The diabetic model was established by intraperitoneally injecting streptozotocin 60 mg/kg.The hearts were rapidly excised and retrogradely perfused with K-H solution saturated with 95% O₂-5% CO₂ at 37 ℃ in a Langendorff apparatus.Sixteen Langendorff-perfused diabetic hearts were divided into 3 groups (n=8 each) using a random number table method: diabetes mellitus group (group D) and sevoflurane group (group DS). Another 8 Langendorff-perfused normal hearts of rats were selected and served as control group (group C). After 15 min equilibration with K-H solution, the hearts were continuously perfused for 30 min with K-H solution in group C and group D and with K-H solution saturated with 2.5% sevoflurane in group DS.S1S2 program-controlled stimulation was performed at the end of perfusion, the occurrence of induced ventricular arrhythmia (VA) and the maximal pacing cycle length (PCL) of induced VA were recorded, and conduction velocity (CV) was calculated.The expression of phosphorylated Cx43 at Ser368 (p-Cx43 Ser368) in ventricular myocytes was determined by Western blot. Results: Compared with group C, the incidence of induced VA was significantly increased, the maximal PCL of induced VA was prolonged, the CV was decreased, and the expression of p-Cx43 Ser368 was up-regulated in group D (P<0.05). Compared with the incidence of induced VA was significantly decreased, the maximal PCL of induced VA was shortened, the CV was increased, and the expression of p-Cx43 Ser368 was down-regulated in group DS (P<0.05). Conclusion The mechanism by which sevoflurane stabilizes the ventricular electrical conduction is associated with decreasing the phosphorylation of Cx43 at Ser368 in diabetic rats.

Objective: To evaluate the electrophysiological changes of atrial myocardium in a rat model of hypothermic ischemia-reperfusion (I/R). Methods: Sixteen isolated Sprague-Dawley rat hearts successfully perfused in the Langendorff apparatus were divided into control group (group C) and hypothermic I/R group (group IR) using a random number table method, with 8 heats in each group.Heats in group IR were further divided into reperfusion-non-atrial arrhythmia subgroup (group R-NAA) and reperfusion-atrial arrhythmia subgroup (group R-AA) depending on whether atrial arrhythmia occurred after reperfusion.In group C, the heart was perfused with K-H solution at 37 ℃ for 120 min.In group IR, the heart was perfused with K-H solution at 37 ℃ for 30 min and then perfusion was stopped, cardiac arrest was induced for 60 min through injecting Thomas solution (4 ℃, 20 ml/kg), the area around the heart was protected with low temperature (4 ℃) Thomas solution, and hearts were resuscitated with 4 ℃ Thomas solution (10 ml/kg) at 30 min after cardiac arrest and with 37 ℃ K-H solution for 30 min staring from 60 min after cardiac arrest.At 30 min of equilibration (T₀), 105 min of equilibration/15 min of reperfusion (T₁), and 120 min of equilibration/30 min of reperfusion (T₂), right atrial monophasic action potentials, maximal velocity of phase zero, monophasic action potential amplitude (MAPA) and MAP duration at 50% and 90% of repolarization (MAPD₅₀ and MAPD₉₀) were measured.Right-atrium conduction velocity and effective refractory period were recorded at T₂, and the ratio of ERP to MAPD₉₀ (ERP/MAPD₉₀) was calculated.Atrial fibrillation was induced by programmed electrical stimulation, and the maximum pacing cycle length of inducing atrial fibrillation (AF-PCL_max) was recorded. Results: Compared with C and R-NAA groups, the maximal velocity of phase zero was significantly decreased and MAPD₉₀ was increased at T₁, the right-atrium conduction velocity and ERP/MAPD₉₀ ratio were decreased and MAPD₉₀, effective refractory period and AF-PCL_max were increased at T₂ in group R-AA (P<0.05). Conclusion The decrease in depolarization velocity, prolongation of repolarization duration and decrease in conduction velocity, excitability and electrical stability may be the electrophysiological mechanism of reperfused atrial arrhythmia in rats.