Objective To investigate the effects of electroacupuncture of different stimulation waveforms on the 5-hydroxytryptamine (5-HT), glutamic acid (Glu) and gamma-aminobutyric acid (CABA) contents of the hypothalamus in rats with para-chlorophenylalanine (PCPA)-induced insomnia and explore the difference in the effects and the mechanism of its action. Methods Fifty SD rats were randomly allocated to a normal group of 10 rats, a model group of 10 rats and an electroacupuncture group of 30 rats. The electroacupuncture group was then randomly divided to electroacupuncture groups 1, 2 and 3, 10 rats each. A rat model of insomnia was made using PCPA in all groups of rats except the normal group. All the electroacupuncture groups received electroacupuncture treatment. Of them, electroacupuncture group 1 received sparse wave treatment; electroacupuncture group 2, dense wave treatment;electroacupuncture group 3, sparse-dense wave treatment. After 6 days of treatment, every group of rats was sacrificed by cervical dislocation. The 5-HT, Glu and CABA contents of the hypothalamus were measured by enzyme-linked immunosorbent assay. Results The 5-HT content of the brain decreased significantly in the model group of rats compared with the blank group (P<0.01) and increased significantly in electroacupuncture group 3 of rats compared with the model group (P<0.01). There was a statistically significant difference in brain 5-HT content between electroacupuncture group 2 or 3 of rats and electroacupuncture group 1 (P<0.05,P<0.01) and between electroacupuncture groups 3 and 2 of rats (P<0.01). The Glu and CABA contents of the cerebral cortex and the ratio of Glu/CABA increased significantly in the model group of rats compared with the blank group (both P<0.01) and decreased significantly in electroacupuncture group 3 of rats compared with the model group (both P<0.01). There were statistically significant differences in the Glu and CABA contents of the cerebral cortex between electroacupuncture group 2 or 3 of rats and electroacupuncture group 1 ((P<0.05,P<0.01) and between electroacupuncture groups 3 and 2 of rats (P<0.01). Conclusions Electroacupuncture can regulate hypothalamic monoamine neurotransmitter 5-HT content and amino acid neurotransmitters Glu and CABA contents and reduce intracerebral amino acid toxicity to produce a therapeutic effect on insomnia in insomnia rats. The therapeutic effect of sparse wave electroacupuncture is superior to that of dense wave or sparse-dense wave electroacupuncture.

OBJECTIVETo investigate whether inhalable particulate matters can cause the damage of chromosome or mitotic apparatus to produce micronucleus, and to evaluate genetic toxicology of moxa smoke on chromosome.

METHODSBy MTT method, the 24 h half maximal inhibitory concentration (IC50) of moxa smoke condensation (MSC) on Chinese hamster ovary (CHO) cells was 0.087 mg/mL. CHO cells, which were cultured in vitro, were divided into a solvent control group, a positive control group (cyclophosphamide as solvent), a low concentration group, a moderate concentration group and a high concentration group. The low concentration group, moderate concentration group and high concentration group were set approximately 1/8, 1/4, 1/2 of IC50, respectively. Whether micronucleus had dose-effect response induced by the damage of chromosome or mitotic apparatus was observed after CHO cells were contaminated by MSC in the low concentration group, moderate concentration group and high concentration group.

RESULTSThe rate of micronucleus induced by MSC in the low concentration group, moderate concentration group and high concentration group was higher than that in the solvent control group (all P < 0.05), which presented dosage-effect response. The experiment was repeated 3 times, indicating it was repeatable with statistical significance.

CONCLUSIONHigh concentration of MSC shows toxicity to induce chromosome damage, which disappears at low concentration. The genetic toxicology is also dependent on concentration, and the concentration of moxa smoke is essential. In clinical treatment, it is noted to control the level of moxa smoke, while the clinical safety standard of moxa smoke concentration is in need of further study.

Air Pollutants ; adverse effects ; Animals ; CHO Cells ; Cell Nucleus ; drug effects ; genetics ; Cricetinae ; Cricetulus ; Inhalation Exposure ; adverse effects ; analysis ; Micronucleus Tests ; Moxibustion ; adverse effects ; Particulate Matter ; adverse effects ; Smoke ; adverse effects ; analysis

OBJECTIVETo observe the effects of intervention of moxa smoke with different concentrations on superoxide dismutase (SOD) and malondialdehyde (MDA) in serum and lung of male rats, so as to explore the safety concentration of moxa smoke.

METHODSA total of 32 Wistar male rats were randomly divided into a control group, a low-concentration group, a moderate-concentration group and a high-concentration group, 8 rats in each one. All the rats were exposed in the full-automatic toxicant exposure cabinet, and the overshadow of moxa smoke was set at 0%, 10%, 40% and 70%, respectively. Each rat was exposed for 20 min per day. After 26 weeks, the activities of SOD and content of MDA in serum, lung organ and bronchoalveolar lavage fluid were tested.

RESULTSCompared with the control group, the activities of serum SOD in the high-concentration group were reduced (P< 0. 05), but those in the low-concentration group and moderate-concentration group were not significantly different (both P>0. 05). Compared with the control group, the content of serum MDA in the low-concentration group, moderate-concentration group and high-concentration group was increased insignificantly (all P>0. 05). There were no significant differences regarding activities of SOD and content of MDA in lung organ and bronchoalveolar lavage fluid among each moxa smoke group (all P>0. 05).

CONCLUSIONThere is no obvious toxic reaction in the low-concentration group and moderate-concentration group; in the high-concentration group the antioxidant ability is damaged due to long-term exposure.

Animals ; Artemisia ; chemistry ; Lung ; enzymology ; metabolism ; Male ; Malondialdehyde ; blood ; metabolism ; Moxibustion ; Rats ; Rats, Wistar ; Smoke ; analysis ; Superoxide Dismutase ; blood ; metabolism

OBJECTIVE: To observe the effects of moxa smoke through olfactory pathway on learning and memory ability in rapid aging (SAMP8) mice, and to explore the action pathway of moxa smoke. METHODS: Forty-eight six-month-old male SAMP8 mice were randomly divided into a model group, an olfactory dysfunction group, a moxa smoke group and an olfactory dysfunction + moxa smoke group, with 12 mice in each group. Twelve age-matched male SAMR1 mice were used as the blank group. The olfactory dysfunction model was induced in the olfactory dysfunction group and the olfactory dysfunction + moxa smoke group by intraperitoneal injection of 3-methylindole (3-MI) with 300 mg/kg, and the moxa smoke group and the olfactory dysfunction + moxa smoke group were intervened with moxa smoke at a concentration of 10-15 mg/m³ for 30 min per day, with a total of 6 interventions per week. After 6 weeks, the emotion and cognitive function of mice was tested by open field test and Morris water maze test, and the neuronal morphology in the CAI area of the hippocampus was observed by HE staining. The contents of neurotransmitters (glutamic acid [Glu], gamma-aminobutyric acid [GABA], dopamine [DA], and 5-hydroxytryptamine [5-HT]) in hippocampal tissue of mice were detected by ELISA. RESULTS: The mice in the blank group, the model group and the moxa smoke group could find the buried food pellets within 300 s, while the mice in the olfactory dysfunction group and the olfactory dysfunction + moxa smoke group took more than 300 s to find them. Compared with the blank group, the model group had increased vertical and horizontal movements (P<0.05) and reduced central area residence time (P<0.05) in the open field test, prolonged mean escape latency on days 1-4 (P<0.05), and decreased search time, swimming distance and swimming distance ratio in the target quadrant of the Morris water maze test, and decreased GABA, DA and 5-HT contents (P<0.05, P<0.01) and increased Glu content (P<0.05) in hippocampal tissue. Compared with the model group, the olfactory dysfunction group had increased vertical movements (P<0.05), reduced central area residence time (P<0.05), and increased DA content in hippocampal tissue (P<0.05); the olfactory dysfunction + moxa smoke group had shortened mean escape latency on days 3 and 4 of the Morris water maze test (P<0.05) and increased DA content in hippocampal tissue (P<0.05); the moxa smoke group had prolonged search time in the target quadrant (P<0.05) and increased swimming distance ratio, and increased DA and 5-HT contents in hippocampal tissue (P<0.05, P<0.01) and decreased Glu content in hippocampal tissue (P<0.05). Compared with the olfactory dysfunction group, the olfactory dysfunction + moxa smoke group showed a shortened mean escape latency on day 4 of the Morris water maze test (P<0.05). Compared with the moxa smoke group, the olfactory dysfunction + moxa smoke group had a decreased 5-HT content in the hippocampus (P<0.05). Compared with the blank group, the model group showed a reduced number of neurons in the CA1 area of the hippocampus with a disordered arrangement; the olfactory dysfunction group had similar neuronal morphology in the CA1 area of the hippocampus to the model group. Compared with the model group, the moxa smoke group had an increased number of neurons in the CA1 area of the hippocampus that were more densely packed. Compared with the moxa smoke group, the olfactory dysfunction + moxa smoke group had a reduced number of neurons in the CA1 area of the hippocampus, with the extent between that of the moxa smoke group and the olfactory dysfunction group. CONCLUSION The moxa smoke could regulate the contents of neurotransmitters Glu, DA and 5-HT in hippocampal tissue through olfactory pathway to improve the learning and memory ability of SAMP8 mice, and the olfactory is not the only effective pathway.
Male ; Animals ; Mice ; Olfactory Pathways ; Smoke/adverse effects* ; Serotonin ; Aging ; Dopamine ; Olfaction Disorders/etiology*