Regulation of Naoxin'an Capsule on Glial Cell Activation and Inflammatory Response in Rats with Chronic Cerebral Hypoperfusion-induced Vascular Cognitive Impairment / 中国实验方剂学杂志

Objective:To investigate the protective effect of Naoxin'an capsule （NC） against glial cell activation and inflammatory damage in brain of rats with chronic cerebral hypoperfusion-induced vascular cognitive impairment （VCI）. Method:One hundred and fifty rats were randomly divided into a sham operation group （<italic>n</italic>=20） and a modeling group （<italic>n</italic>=130）. Following the modeling with the two vessels occlusion （2-VO） technique， 87 successfully modeled rats were randomly divided into the model group， positive drug group （aricept， 0.5 mg·kg^-1）， and low-， medium-， and high-dose （0.18， 0.36， 0.72 g·kg^-1） NC groups， with 17-18 rats in each group. After intragastric administration of NC for eight weeks， the Morris water maze test and passive avoidance test were conducted to detect the effects of NC on learning and memory ability of VCI rats. Changes in neuronal structure of rat hippocampal CA1 area were observed by hematoxylin-eosin （HE） staining， and the neuronal apoptosis in hippocampus by terminal deoxynucleotidyl transferase （TdT）-mediated dUTP nick end labeling （TUNEL） staining. Western blot assay was used to detect the expression levels of glial fibrillary acidic protein （GFAP）， ionized calcium-binding adapter molecule 1 （Iba-1）， phosphorylated p38 mitogen-activated protein kinase （p38 MAPK）， and phosphorylated nuclear factor <italic>κ</italic>B （NF-<italic>κ</italic>B）， followed by the measurement of interleukin-1<italic>β</italic> （IL-1<italic>β</italic>） and tumor necrosis factor-<italic>α</italic> （TNF-<italic>α</italic>） in the brain by enzyme-linked immunosorbent assay （ELISA）. Result:Compared with the sham operation group， the model group displayed obviously decreased spatial learning and memory ability and memory retention ability （<italic>P</italic><0.05， <italic>P</italic><0.01）， neuronal damage in hippocampal CA1 area， enhanced neuronal apoptosis （<italic>P</italic><0.01）， up-regulated GFAP and Iba-1 （<italic>P</italic><0.01）， elevated phosphorylation of p38 MAPK and NF-<italic>κ</italic>B （<italic>P</italic><0.01）， and increased IL-1<italic>β</italic> and TNF-<italic>α</italic> （<italic>P</italic><0.01）. Compared with the model group， NC at each dose significantly improved the spatial learning and memory ability and memory retention ability of VCI rats （<italic>P</italic><0.05， <italic>P</italic><0.01）， ameliorated the neuronal damage in hippocampus CA1 area， reduced the apoptosis rate of nerve cells （<italic>P</italic><0.05， <italic>P</italic><0.01）， down-regulated the expression of GFAP and Iba-1 （<italic>P</italic><0.01）， decreased the phosphorylation levels of p38 MAPK and NF-<italic>κ</italic>B （<italic>P</italic><0.05， <italic>P</italic><0.01）， and lowered TNF-<italic>α</italic> and IL-1<italic>β</italic> levels （<italic>P</italic><0.01）. Conclusion:NC alleviates the inflammatory damage of the central nervous system caused by activated p38 MAPK and NF-<italic>κ</italic>B and improves chronic cerebral hypoperfusion-induced VCI in rats by inhibiting the activation of microglia and astrocytes.

Pharmacological activity of Terminalia chebula / 中国中药杂志

Terminalia chebula Retz, known as the "king" of Mongolian and Tibetan medicines, is a drug for a wide range of diseases. The main chemical components of myrobalan include triterpene acid, galloyl glucose, anthraquinonoid. The modern pharmacological studies show that myrobalan has multiple biological activities, including antimicrobial, anti-inflammatory, antioxidation as well as anti-tumor. Based on domestic and foreign literatures in recent years, this paper gave a review on the advance of studies for pharmacological activity of T. chebula. and its active components, so as to provide a reference for the in-depth studies on the pharmacological action of myrobalan, and the further development and utilization of myrobalan.

Sacrococcygeal gap injection for the treatment of failed back surgery syndrome / 中国骨伤

<p><b>OBJECTIVE</b>To explore the clinical effect of the sacrococcygeal space injection for the treatment of failed back surgery syndrome.</p><p><b>METHODS</b>From July 1998 to October 2012,47 patients with failed back surgery syndrome were treated and included 39 males and 8 females with an average age of 61.5 years old ranging from 35 to 89 years old. Among them,41 patients experienced one time of operation, 6 patients with twice of operation. Forty-one patients underwent single,bilateral fenestration or central laminectomy decompression, discectomy. Six patients underwent total laminectomy discectomy and inter body fusion and pedicle screw fixation. All patients were examined by X-ray plain film, CT or MRI before treatment. The anticoagulation was discontinuation before treatment. The needle was put into the sacrococcygeal gap at prone position in the sense of frustration,suction without cerebrospinal fluid and blood,with injection of Mailuoning (Chinese characters: see text) 15 ml. The pain was assessed by VAS before and after treatment. The Oswestry low back pain disability index and survival quality interference degree were evaluated.</p><p><b>RESULTS</b>At 1 month after treatment,the pain VAS decreased from 59.24 +/- 17.35 before treatment to 19.19 +/- 11.19 after treatment (P < 0.05); The Oswestry low back pain disability index decreased from (41.35 +/- 9.87)% before treatment to (23.17 +/- 17.56)% after treatment (P < 0.05); The survival quality interference degree decreased from 6.5 +/- 2.2 before treatment to 2.6 +/- 1.4 after treatment (P < 0.05).</p><p><b>CONCLUSION</b>The sacrococcygeal gap injection for treatment of failed back surgery syndrome has advantages of simple, safe, fewer complications, and low treatment cost.</p>

Discovery of N-(3,5-bis(1-pyrrolidylmethyl)-4-hydroxybenzyl)-4-methoxybenzenesulfamide (sulcardine) as a novel anti-arrhythmic agent.

AIM: To investigate the anti-arrhythmic effects of sulfamide analogues of changrolin and to characterize the sulfate of compound 6f (sulcardine sulfate, Sul) as a novel anti-arrhythmic agent. METHODS: The anti-arrhythmic effects of compounds were studied against aconitine-induced arrhythmias in rats and ouabain-induced arrhythmias in guinea pigs. The effects of Sul on transmembrane action potentials were investigated in isolated rabbit sinoatrial nodes and guinea-pig papillary muscles using intracellular recording. With a whole-cell recording technique, the effects of Sul on sodium current, calcium current, and potassium currents were examined in isolated single guinea-pig ventricular myocytes. RESULTS: In aconitine-induced arrhythmias of rats, sulfamide analogues of changrolin (4, 5, and 6a-6p) exhibited various anti-arrhythmic activities. The sulfate of compound 6f (Sul) increased the amount of aconitine required to induce arrhythmias in each treated animal. The ED50 value of Sul in rats was 196 mg/kg. In ouabain-induced arrhythmias of guinea pigs, 25, 50, and 100 mg/kg doses of Sul increased the dose of ouabain required to induce VP, VT, and VF in a dose-dependent manner. In papillary preparations, Sul produced a concentration-dependent decrease in APA and V(max), prolonged APD(90) and ERP, whereas RP was unaffected. In the spontaneously beating sinus nodes, Sul reduced APA and V(max) in a concentration-dependent manner. The whole-cell recording studies revealed that Sul produced a reversible reduction in I(Na) (IC50=26.9 µmol/L) and I(Ca,L)(IC50=69.2 µmol/L), whereas the inward rectifier (I(K1)) and the delayed rectifier potassium currents (I(K)) were unaffected. CONCLUSION: As a multi-ion channel blocker, Sul may have potent efficacy in anti-atrial and ventricular arrhythmias.