ABSTRACT
Objective:To observe the effects of electroacupuncture (EA) on expression of phosphatidylinositol 3 kinase/glycogen synthase kinase 3 alpha (PI3K/GSK3α) signaling pathway related proteins in cortex of APP/PS1 double transgenic mice, and the senile plaque (SP) deposit. Methods:Three-month-old male APP/PS1 mice were randomly divided into model group (n = 6) and EA group (n = 6) after gene identification, and other six wild C57 mice were as control group. EA group accepted EA at Baihui (GV20) and bilateral Shenshu (BL23) for 14 days. Then, the amount of SP in cortex, the expression of P85α and P110α, subunits of PI3K, and GSK3α and pS21-GSK3α, were detected with Western blotting and immunohistochemistry. Results:The SP increased in the model group compared with that of the control group (P < 0.001), and it decreased in EA group compared with that of the model group (P < 0.001). All the proteins expressed in the cytoplasm of cortical neurons. The expression of pS21-GSK3α, P110α and P85α decreased in the model group compared with that of the control group (P < 0.01), while the expression of GSK3α increased (P < 0.05). The expression of pS21-GSK3α, P110α and P85α increased in EA group compared with that of the model group (P < 0.01), while the expression of GSK3α decreased (P < 0.05). Conclusion:EA may adjust the PI3K/GSK3α signaling pathway, to reduce the formation and deposition of SP in APP/PS1 double-transgenic mice.
ABSTRACT
OBJECTIVE@#To observe the effect of electroacupuncture (EA) on the expression of insulin phosphatidylinositol-3 kinase/glycogen synthetase kinase-3α (PI3K/GSK3α) signal pathway related proteins in the hippocampus in mice with Alzheimer's disease (AD), and to explore the regulatory mechanism of EA on improving the pathological characteristics of AD.@*METHODS@#Twelve male APP/PS1 double transgenic mice were randomly divided a model group and a treatment group, 6 mice in each group; another 6 wild-type male mice were taken as the control group. The mice in the treatment group were treated with EA (continuous wave, 2 Hz of frequency) at "Baihui" (GV 20) and bilateral "Shenshu" (BL 23), once a day; 7-day treatment was taken as a course of treatment, and 2 courses of treatment were given. The immunohistochemistry method and Western blot method were used to detect the distribution and expression level of hippocampal PI3K/GSK3α signal pathway related proteins P85α, P110α, GSK3α and pSGSK3α, and the number of hippocampal senile plaques (SP) was observed.@*RESULTS@#The proteins of P85α, P110α, GSK3α and pSGSK3α were mainly distributed in the cytoplasm of hippocampal neurons, and the GSK3α was also distributed in the axons of neurons in the model group and the treatment group. The immunohistochemistry results showed that the distribution level of GSK3α in the hippocampus in the model group was significantly higher than that in the control group (<0.001), and the distribution level of pSGSK3α, P85α and P110α was significantly decreased (<0.01, <0.001); compared with the model group, the distribution level of GSK3α in the hippocampus in the treatment group was significantly decreased (<0.001), and the distribution level of pSGSK3α, P85α and P110α in hippocampus was significantly increased (<0.05, <0.001). The Western blot results showed compared with the control group, the expression of pSGSK3α, P85α and P110α as well as the ratio of pSGSK3α/GSK3α in the hippocampus in the model group were significantly decreased (<0.001), and the expression of GSK3α was increased (<0.05); compared with the model group, the expression of pSGSK3α, P85α, P110α and the ratio of pSGSK3α/GSK3α in the hippocampus in the treatment group were significantly increased (<0.01, <0.001), and the expression of GSK3α was decreased (<0.05). Compared with the control group, the number of hippocampal SP in the model group was significantly increased (<0.001); compared with the model group, the number of hippocampal SP in the treatment group was significantly decreased (<0.01).@*CONCLUSION@#EA could effectively regulate the expression of PI3K/GSK3α signal pathway related proteins in the hippocampus in mice with AD, so as to reduce the formation and deposition of SP.
Subject(s)
Animals , Male , Mice , Alzheimer Disease , Therapeutics , Electroacupuncture , Hippocampus , Physiology , Insulin , Physiology , Mice, Transgenic , Random Allocation , Signal TransductionABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of androgen receptor (AR) on IgG protein expression and the proliferation and migration of prostate cancer cells.</p><p><b>METHODS</b>Western blotting was used to detect the expression of AR protein and IgG in androgen-dependent prostate cancer LNCap cells and castration-resistant prostate cancer PC-3 cells. In AR-overexpressing cells (PC-3-AR cells) established by transfecting PC-3 with AR gene (pCDNA3.1) and LNCap cells with small interfering RNA-mediated AR silencing (LNCap-siAR cells) were analyzed for expressions of AR protein and IgG with Western blotting; the expression of IgG mRNA was detected by Q-PCR, and the cell proliferation and migration were assessed with MTT assay and wound healing assay, respectively.</p><p><b>RESULTS</b>Compared with PC-3 cells, LNCap cells expressed a higher level of AR protein and a lower level of IgG (P<0.05). PC-3-AR cells showed attenuated proliferation and migration with a lowered expression of IgG (P<0.01), while LNCap-siAR cells showed enhanced proliferation and migration with increased expression of IgG (P<0.01).</p><p><b>CONCLUSION</b>The expression of AR is inversely correlated with IgG and is associated with the proliferation and migration of prostate cancer cells in vitro.</p>