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Aim: To observe the iconography and biomechanical changes of femur in this D-galactose induced osteoporosis model in male mice, using Micro CT and other methods, and to observe the effect of calcitriol in this model. Methods: Thirty SPF male KM mice of 17 weeks old were randomly divided into control group, model group and calcitriol group, and the drug administration lasted for 12 weeks. At the end of the experiment, the mice were sacrificed and the bilateral femurs were taken for a bio-mechanical three-point bending test and a Micro CT scan. Results: Compared with control group, the Micro CT index of the femur in model group showed that Conn. D., BMD, BV/TV and Tb. N were significantly reduced (P < 0. 05), and SMI was raised significantly (P < 0. 05). Compared with model group, the BMD, BV/TV, Tb. N and Tb. Th in calcitriol group were significantly raised (P <0. 05), and SMI was significantly reduced (P < 0. 05). What's more, the break load, elastic load, maximum load and stiffness coefficient in calcitriol group significantly increased (P < 0. 05). Conclusions: D-galactose can induce a visible iconography changes of osteoporosis in male mice. Calcitriol can significantly improve the micro structure of trabecular bone and increase the bio-mechanical properties of femur in D-galactose male mice.
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Objective To investigate the effects of Bushen Huoxue acupuncture method on the behavioral changes and the proliferation of endogenous neural stem cells (NSCs) in hippocampus of Alzheimer disease (AD) model mice. Methods 18 male SAMP8 mice, seven months old, were randomly divided into acupuncture group, non-acupoint control group, and model control group. And another age-matched 6 male SAMR1 mice were prepared as normal control group. Mice in acupuncture group were intervened by acupuncture method in the acupoints of "Shenshu", "Baihui", "Xuehai", and "Geshu". Mice in non-acupoint control group were treated by stimulating the fixed non-point under the bilateral rib, while mice in model control group and normal control group were raised without special treatment but administered the stimulation of catching with the same time and the same stimulus intensity. All treatrment lasted for 8 weeks. After the intervention, the learning and memory abilitities and brain hippocampus Brd U positive cells of all groups were detected. Results Compared with the nomal control group, mice in the model control group had longer escape latency and less time spent in former platform quadrant (P＜0.05); the number of Brd U positive cells decreased significantly (P＜0.05). Compared with the model control group and the non-acupoint control group, mice in the acupuncture group had shorter escape latency and more time spent in former platform quadrant (P＜0.05); the number of Brd U positive cells increased significantly (P＜0.05). Conclusion Bushen Huoxue acupuncture method can improve the learning and memory abilities of SAMP8 mice AD model by inducing the proliferation of hippocampal endogenous NSCs.
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Objective:To observe the effect of acupuncture on the expression of mitochondrial proteome in hippocampus of senescence-accelerated mouse prone g (SAMPg) mice models with Alzheimer disease (AD),and to explore the possible protective mechanism of acupuncture on mitochondria.Methods:Sixty 6-month-old male SAMP8 mice were randomly divided into an acupuncture at acupoint group,an acupuncture at non-acupoint group and a model group,20 mice in each group.The 20 male senescence-accelerated mouse/resistance 1 (SAMR1) mice of the same age were used as a normal control group.Shenshu (BL 23),Baihui (GV 20),Xuehai (SP 10) and Geshu (BL 17) were selected for acupuncture intervention in acupuncture at acupoint group.After an 8-week intervention,mitochondrial tissues were extracted from the hippocampus.Differentially expressed proteins were identified by subcellular organelle proteomics.Western blot was used to verify the expressions of some related proteins in hippocampal mitochondria.Results:Compared with the model group,there were 13 differentially expressed protein spots in the acupuncture at acupoint group,of which,9 were up-regulated,including neurofilament light polypeptide (NFL),actin (cytoplasmic 1,database ID:ACTB),tubulin beta-2A chain (TBB2A),tropomodulin-2 (TMOD2),pyruvate dehydrogenase E1 component subunit beta (PDHE1-β),NADH-ubiquinone oxidoreductase 75 kDa subunit (database ID:NDUS1),heat shock cognate 71 kDa protein (HSC71),pyruvate dehydrogenase E1 component subunit alpha (PDHE1-α) and ATP synthase beta subunit (ATP-β);4 were down-regulated,including glial fibrillary acidic protein (GFAP),pyruvate dehydrogenase phosphatase 1 (PDP1),mitochondrial-processing peptidase subunit alpha (MMP-α) and adenosine kinase (ADK).According to the information provided in the protein database,most of the differentially expressed proteins involve the regulation of mitochondrial function and structure.The expression levels of NFL and TBB2A in the normal control group and the acupuncture at acupoint group were significantly higher than those in the acupuncture at non-acupoint group (P＜0.05).ATP-β and NDUS1 expression levels were significantly higher in the acupuncture at acupoint group than those in the acupuncture at non-acupoint group (P＜0.05);there was no significant difference between the acupuncture at non-acupoint group and the model group (P＞0.05).Conclusion:Acupuncture may achieve the potential therapeutic effect on AD by regulating the structure and functional proteins of hippocampal mitochondria.
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Objective To observe the effects of Bushen Huoxue acupuncture method on amygdaloid protein expression in SAMP8; To explore the potential target protein for acupuncture treatment of Alzheimer disease (AD). Methods Thirty six-month-old male SAMP8 mice were randomly divided into acupuncture group and control group, 15 mice in each group. Acupuncture group selected Baihui (GV20), Shenshu (BL23), Geshu (BL17) and Xuehai (SP10) to intervene. The control group was given the same time to catch and stimulate. After 8 weeks, the amygdala was extracted and the differential expression protein spots were identified by proteomic techniques. Results Compared with control group, acupuncture group eventually identified 9 differential expression protein spots, of which 6 up-regulated and 3 down-regulated. According to the relevant information provided in the protein database, the main function of differential expression proteins involved in the mitochondrial energy metabolism, oxidative stress, and production of Aβ. Conclusion Bushen Huoxue acupuncture method can regulate multiple protein expressions in amygdala, suggesting that it may be through improving mitochondrial energy metabolism, oxidative stress, reducing production of Aβ to realize the potential therapeutic effects on AD.
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Objective To observe the effects of acupuncture on the behaviors and the expressions of Fis1 and OPA1, as well as mitochondrial ultrastructure in the hippocampus of mice with Alzheimer disease (AD); To explore the mechanism of action of acupuncture for AD.Methods Forty male SAMP8 mice were randomly divided into acupuncture group and model group, with 20 mice in each group. Another 20 male natural aging mice with the same age (SAMR1 mice) were set as the normal group. Acupuncture group chose Shenshu, Baihui, Xuehai and Geshu for intervention. 8 weeks later, Morris water maze was used to test the mice behaviors, and then hippocampus organization was taken. Western blot was used to detect the expressions of Fis1 and OPA1 and mitochondrial ultrastructure in hippocampal neurons of mice was observed by transmission electron microscopy.Results Compared with the model group, the escape latency of acupuncture group was significantly shortened (P<0.05), and the stay time in the former platform quadrant and former platform crossing times were significantly increased (P<0.05). The expression of Fis1 in the hippocampus of acupuncture group decreased significantly (P<0.05), while the expression of OPA1 increased significantly (P<0.05). The mitochondrial ultrastructure in hippocampus in the acupuncture group was effectively improved, and the mitochondrial surface density and body density were both increased in the acupuncture group compared with the model group (P<0.05).Conclusion Acupuncture may play a potential therapeutic role in AD by decreasing the expression of Fis1, increasing the expression of OPA1, recovering the injury of mitochondrial ultrastructure.
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Objective To investigate the effect of acupuncture on behaviors and its mechanism of action in a SAMP8 mouse model of Alzheimer disease.Methods Sixty 6-month-old male SAMP8 mice were randomized to acupuncture,model and non--acupoint groups.Twenty male SAMP 1 mice of the same age constituted a normal control group.The acupuncture group received intervention by acupuncture at Shenshu,Baihui,Xuehai and Geshu.After eight weeks,a behavioral test was performed using the Morris water maze in every group of mice.The expressions of Flotillin-1,NEP and Aβ42 in mouse hippocampus were determined by western blot.Results The Morris water maze test showed that as compared with the model group,escape latency shortened significantly (P＜0.05) and the time spent in the former platform quadrant and the number of former platform position crossings increased (P＜0.05) in the acupuncture group of mice;escape latency,the time spent in the former platform quadrant and the number of former platform position crossings had no significant differences in the non-meridian-acupoint group of mice (all P＞0.05).As compared with the model group,Flotillin-1 expression decreased significantly in the acupuncture group (P＜0.05) but had no significant difference in the non-meridian-acupoint group (P＞0.05);NEP expression increased significantly in the acupuncture group (P＜0.05) but had no significant difference in the non-meridian-acupoint group (P＞0.05);Aβ42 expression decreased significantly in the acupuncture group (P＜ 0.05) but had no significant difference in the non-meridian-acupoint group (P＞0.05).Conclusions Acupuncture can markedly improve learning and memory abilities in a SAMP8 mouse model of AD and reduce Flotillin-1 content and upregulate NEP expression in SAMP8 mouse hippocampus to decrease Aβ42 expression,relieve neurotoxicity and produce a neuroprotective effect.