OBJECTIVE[corrected] To characterize the insulinotropic action of hippocampal cholinergic neurostimulating peptide (HCNP) and analyze the role of type 3 muscarinic receptor (M(3)R) pathway in the action of HCNP.

METHODSINS-1 cells were incubated in routine RPMI 1640 medium (control group), RPMI 1640 supplemented with 50 pg/ml synthetic HCNP (HCNP group), or HCNP-containing medium with the addition of PMA 18 h prior to insulin release assay. The insulin levels in the medium was measured using radioimmunoassay following stimulation with different concentrations of glucose. Real-time quantitative PCR was used for detecting the gene expression of HCNP-pp, choline acetyltransferase (ChAT) and M(3)R in HCNP group and control group.

RESULTSAfter stimulation with different concentrations of glucose (5.6 and 16.7 mmol/L), HCNP group showed significantly higher insulin levels than the control and HCNP+ PMA groups. Compared with those in the control group, the mRNA levels of HCNP-pp, ChAT, and M(3)R were all lowered in HCNP group.

CONCLUSIONHCNP can promote insulin release in INS-1 cells by increasing ChAT activity and activating M(3)R, and this effect is inhibited by PMA.

Animals ; Cell Line ; Insulin ; secretion ; Neuropeptides ; pharmacology ; Rats ; Receptor, Muscarinic M3 ; metabolism

AIMTo investigate the effects of calcitonin gene-related peptide (CGRP), gastrin 17 (G17), bombesin (Bom), met-enkephalin (Met-enk), neuropeptide Y (NPY) and somatostatin (SS) on GMBF and the role of endogenous NO in increased GMBF induced by neuropeptides in rats.

METHODSBy hydrogen gas clearance technique to measure gastric mucosal blood flow (GMBF) and arterial infusion close to stomach or intracerebroventricular (icv) to microinject neuropeptides.

RESULTS(1) Arterial infusions of CGRP and G17 (5, 50 and 100 pmol x min(-1)) increased GMBF significantly in dose-dependent manners. CGRP had more effective effect on increasing GMBF than that of G17. Intravenous pretreatment of L-nitro-L-arginine methyl ester (L-NAME) to inhibit the synthesis of endogenous NO could abolish completely or partially the increases in GMBF response to CGRP or G17 respectively. (2) Arterial infusions of Bom and Met-enk (50 and 100 pmol x min(-1)) increased GMBF significantly. The increases in GMBF induced by Bom or Met-enk were abolished completely or partially by pretreatment of L-NAME respectively. (3) Arterial infusion of NPY (5, 50 and 100 pmol x min(-1)) led to reduction of GMBF significantly in a dose-dependent manner. SS (50 and 100 pmol x min(-1)) also reduced GMBF significantly. (4) icv microinjection of CGRP (10 microg) and G17 (10 Microg) increased GMBF significantly. The increases in GMBF induced by icv microinjection of CGRP or G17 were blocked completely or partially respectively by pretreatments with L-NAME. (5) icv microinjection of NPY (10 microg) decreased GMBF significantly.

CONCLUSIONNeuropeptides play important roles in the regulation of GMBF in rats and NO is involved in the increase of GMBF induced by some neuropeptides.

Animals ; Gastric Mucosa ; blood supply ; drug effects ; Male ; Neuropeptides ; pharmacology ; physiology ; Nitric Oxide ; physiology ; Rats ; Rats, Sprague-Dawley

With the fast development of medicinal animals as new drugs, research on Periplaneta americana become hot recently. Several drugs which mainly consisted of P. americana were approved for clinical applications. The chemical constituents and pharmacological bioactivities of this insect were summarized herein, which provides informativon for further researches on this medicinal animal.
Amino Acids ; isolation & purification ; pharmacology ; Animals ; Anti-Bacterial Agents ; pharmacology ; Antineoplastic Agents ; pharmacology ; Cardiotonic Agents ; pharmacology ; Cycloparaffins ; isolation & purification ; pharmacology ; Materia Medica ; isolation & purification ; pharmacology ; Molecular Structure ; Neuropeptides ; isolation & purification ; pharmacology ; Periplaneta ; chemistry

Animals ; Disease Models, Animal ; Hypoglycemia ; chemically induced ; metabolism ; Hypothalamus ; drug effects ; metabolism ; Insulin ; pharmacology ; Intracellular Signaling Peptides and Proteins ; metabolism ; Male ; Neuropeptides ; metabolism ; Orexins ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo study the effect of ligustrazine on the migration of neuronal precursors (NPs) after focal cerebral ischemia in adult rats and explore its acting mechanism on recovery of function.

METHODSRat model of left middle cerebral artery occlusion (MCAO) was established by thread ligation. Ligustrazine 40 mg/kg was injected peritoneally once a day 2 h after modeling. On the 3rd, 7th, 14th and 21st day after operation, the migration of Doublecortin (DCX, the marker of NPs) in subventricular zone (SVZ) and the rostral migratory stream (RMS) were observed with immunohistochemistry.

RESULTSThe migration of DCX-positive cells in SVZ (abbrev. as migration below) through RMS into the olfactory bulb started from the 3rd day after ischemia, and lasted to the 21st day; the migration directly or through RMS into the ischemic penumbra of the adjacent striatum started on the 7th day, and increased significantly on the 14th day; and a few of DCX positive cells migrated through corpus callosum into the ischemic cortex on the 21st day. The migration was similar in the two groups in its pathway, but the extent in the ligustrazine group was more intensive.

CONCLUSIONLigustrazine could promote direct migration of NPs into the ischemic cerebral cortex and striatum, suggesting that it might play an important role in promoting self-recovery of brain function after ischemia through accelerating the migration of NPs.

Animals ; Anti-Inflammatory Agents, Non-Steroidal ; pharmacology ; Brain Ischemia ; physiopathology ; Cell Movement ; drug effects ; Immunohistochemistry ; Male ; Microtubule-Associated Proteins ; biosynthesis ; Neurons ; drug effects ; metabolism ; pathology ; Neuropeptides ; biosynthesis ; Pyrazines ; pharmacology ; Rats ; Rats, Sprague-Dawley

AIMThe present study was designed to determined the cardiovascular effects of IMD1-53 in rats and its possible mechanism.

METHODSIsolated rat hearts were perfused by Iangendorff mode, and ventricular function was measured after IMD1-53 perfusion. Meanwhere, we investigated the effects of IMDI) on arterial pressure after intravenous administration of IMD. And cAMP content was detected in rat ventricular and aortic tissues.

RESULTSThe results showed that perfusion with IMD significantly enhanced cardiac function and resulted in higher LVSP, +dp/dt(max) and -dp/dt(max) by 45%, 51% and 37%, respectively, compared with control and increased coronary infusion flow. The effects of IMD1-53 on cardiac function were antagonized by H-89, an inhibitor of PKA. The content of cAMP in the ventricular tissues after IMD perfusion was 131% higher than control. In addition, intravenous administration of IMD induced a potent decrease in arterial pressureand heart rate, and in aortic tissues, IMD incubation resulted in a 236% increase in cAMP content compared with control group.

CONCLUSIONThe study reveals that IMD can increase cardiac function and decrease arterial pressure in rat and the effects may be related to cAMP pathway.

Adrenomedullin ; metabolism ; pharmacology ; Animals ; Blood Pressure ; drug effects ; Cardiovascular Physiological Phenomena ; drug effects ; Cyclic AMP ; metabolism ; Heart ; drug effects ; In Vitro Techniques ; Male ; Neuropeptides ; metabolism ; pharmacology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Ventricular Function ; drug effects

OBJECTIVETo observe the effect of orexin-A on the recovery and cognitive function of aged rats after ketamine anesthesia.

METHODSFifty-five aged rats were divided randomly into control group, model control group, 1 nmol/L Orexin-A group, and 4 nmol/L Orexin-A group. In the latter 3 groups, the rats received an intraperitoneal injection of ketamine at 100 mg/kg, and normal saline was injected in the control group. Ten minutes after the injections, the rats received intraventricular injections of artificial cerebrospinal fluid (control and model control group) or of 10 microl 1 or 4 nmol/L Orexin-A as indicated. The behavioral changes of the rats were assessed by the duration of loss of righting reflex (LORR). Electroencephalogram (EEG) recordings were used to evaluate the changes in rat brain activity by comparison of the percent of sigma wave in EEG before and after the intraventricular injections. Morris water maze was used to test the learning and spatial localization abilities of the rats.

RESULTSKetamine resulted in obvious impairment of learning and memory abilities of the aged rats. Orexin-A at 4 nmol/L induced significant decrease in the duration of LORR and marked reduction of sigma activities in anesthetic rats (P<0.05), and obviously improved the learning and spatial localization abilities of the rats after anesthesia (P<0.05).

CONCLUSIONOrexin-A can promote the recovery and improve the cognitive function of aged rats after ketamine anesthesia.

Aging ; Anesthesia Recovery Period ; Anesthetics, Dissociative ; Animals ; Cognition ; drug effects ; Delayed Emergence from Anesthesia ; prevention & control ; Intracellular Signaling Peptides and Proteins ; pharmacology ; Ketamine ; Male ; Neuropeptides ; pharmacology ; Orexins ; Random Allocation ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo explore the effect of soy isoflavone on obesity in the light of hypothalamus and peripheral orexigenic gene regulation.

METHODSFifty-four female rats were randomly assigned to 6 groups: one sham-operated group (SHAM), one ovariectomized (OVX) control group, three OVX groups fed with 400 ppm (L-SI), 1200 ppm (M-SI) and 3600 ppm (H-SI) isoflavone respectively, and one OVX group receiving 0.45 ppm diethylstilbestrol (EC). All rats were allowed to take high-fat diet for 4 weeks. Some neuropeptides were measured by RT-PCR. These neuropeptides included NPY, pro-opiomelanocortin (POMC), cocaine and amphetamine regulated transcript (CART), orexin, melanin-concentrating hormone (MCH), melanin-concentrating hormone precursor (P-MCH), ghrelin, and leptin.

RESULTSCompared with the OVX control group, the body weight and food intake in the H-SI group were reduced significantly and there was a significant dose-dependent manner in the 3 isoflavone groups. The results of RT-PCR showed that the NPY level in the 3 isoflavone groups was significantly increased and the POMC/CART gene expression decreased significantly in rats' hypothalamus compared with that in the OVX control group. However, the expression of orexin, MCH and P-MCH had no change. The peripheral grelin mRNA expression was higher in the 3 isoflavone groups, while leptin gene expression in the fat was not consistent.

CONCLUSIONSThis research showed that isoflavone could prevent obesity induced by high-fat diet and ovariectomy through regulating hypothalamus and peripheral orexigenic gene expressions associated with food intake.

Animals ; Dietary Fats ; pharmacology ; Feeding Behavior ; drug effects ; physiology ; Female ; Gene Expression Regulation ; drug effects ; Hypothalamus ; Isoflavones ; chemistry ; pharmacology ; Neuropeptides ; genetics ; metabolism ; Obesity ; Ovariectomy ; RNA, Messenger ; genetics ; metabolism ; Rats ; Soybeans ; chemistry

Brain ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; Gene Expression ; Neuropeptides ; biosynthesis ; genetics ; Proto-Oncogene Proteins c-fos ; biosynthesis ; genetics ; Proto-Oncogene Proteins c-jun ; biosynthesis ; genetics ; RNA, Messenger ; biosynthesis ; genetics

AIMIn order to study the effects of pituitary adenylate cyclase activating polypeptide(PACAP) on brain edema induced by ischemia in rats and its underlying receptor mechanism.

METHODSBrain ischemia model in rats was established by ligaturing four--vessels. The percentage ratio of wet over dry tissue weight, sodium and potassium contents of dry brain tissue were measured by weighing and enzymatic analysis methods.

RESULTSThe brain water contents significantly increased after rats exposed to 1 h of reperfusion following 30 - minute ischemia. Furthermore, sodium contents in brain tissue increased and potassium contents decreased following perfusion. Changes of brain water contents, sodium and potassium contents were relieved by lateral ventricular injection of PACAP in the concentration of 1 x 10(-9), 1 x 10(-10) or 1 x 10(-11) mol respectively before ischemia. The effect of PACAP could be blocked by MCAP6 - 38 (specific type I PACAP receptor antagonist) lateral ventricular injection prior to PACAP administration.

CONCLUSIONExogenous PACAP may act as a protective effect in brain edema induced by ischemia in rats, which is mediated by type I receptor.

Animals ; Brain ; metabolism ; physiopathology ; Brain Edema ; etiology ; metabolism ; prevention & control ; Brain Ischemia ; complications ; metabolism ; Male ; Neuropeptides ; metabolism ; Pituitary Adenylate Cyclase-Activating Polypeptide ; pharmacology ; Potassium ; metabolism ; Rats ; Rats, Sprague-Dawley ; Sodium ; metabolism