ABSTRACT
Objective:To evaluate the role of hippocampal hemeoxygenase-1 (HO-1) in electroacupuncture (EA)-induced reduction of lipopolysaccharide (LPS)-induced brain injury in mice.Methods:Twenty-four healthy adult C57BL/6J mice of both sexes, weighing 18-22 g, were divided into 4 groups ( n=6 each) using a random number table method: control group (group C), LPS-induced brain injury group (LPS group), LPS plus EA group, and LPS plus EA plus HO-1 inhibitor zinc protoporphyria (ZnPP) group (LPS+ EA+ ZnPP group). A virus carrying calcium ion fluorescent probes was injected into and an optical fiber was implanted into the hippocampal CA1 region to record changes in the calcium fluorescence signals.Three weeks later, Baihui, Quchi and Zusanli acupoints were stimulated with constant voltage (2/15 Hz) and disperse-dense waves for 30 min once a day for 5 consecutive days, and the stimulation intensity was defined as less than 1 mA causing slight muscle contraction.ZnPP 50 μmol/kg was intraperitoneally injected at 12 h before each stimulation in LPS+ EA+ ZnPP group, and the equal volume of normal saline was given instead in the other groups.After the end of EA stimulation on the last day, LPS 5 mg/kg was intraperitoneally injected to induce brain injury.Open field tests were performed at 1 day after LPS injection to record the number of rearing and amplitude of neuronal calcium signals during rearing.Novel object recognition tests were conducted at 3 days after LPS injection, and the exploration index and amplitude of neuronal calcium signals while exploring novel objects were recorded.The mice were sacrificed after the end of behavioral testing, and the brain tissues were obtained and stained by Nissl, and the neurons in the hippocampal CA1 region were counted. Results:Compared with group C, the number of rearing and amplitude of calcium signals in neurons in the hippocampal CA1 region during rearing were significantly decreased, the exploration index and amplitude of calcium signals in neurons in the hippocampal CA1 region while exploring novel objects were decreased, and the neuron counts were reduced in LPS, LPS+ EA and LPS+ EA+ ZnPP groups ( P<0.05 or 0.01). Compared with group LPS, the number of rearing and amplitude of calcium signals in neurons in the hippocampal CA1 region during rearing were significantly increased, and the exploration index and amplitude of calcium signals in neurons in the hippocampal CA1 region while exploring novel objects were increased in group LPS+ EA ( P<0.05), and no significant change was found in the parameters mentioned above in group LPS+ EA+ ZnPP ( P>0.05). Compared with group LPS+ EA, the number of rearing and amplitude of calcium signals in neurons in the hippocampal CA1 region during rearing were significantly decreased, and the exploration index and amplitude of calcium signals in neurons in the hippocampal CA1 region while exploring novel objects were decreased in group LPS+ EA+ ZnPP ( P<0.05). Conclusion:The mechanism by which EA reduces LPS-induced brain injury is related to the activation of the endogenous protective mechanism HO-1 in mice.
ABSTRACT
This paper introduces the failure phenomenon, failure analysis, maintenance process and method of SIEMENS PRIMUS linear accelerator.