1.Effects of Electroacupuncture at Baihui (DU20) on Learning and Memory and Expression of Brain-derived Neu-rotrophic Factor in APP/PS1 Double-transgenic Mice
Jixiang CHEN ; Yunan WU ; Yaxuan ZHENG ; Peiyuan ZHUO ; Yingzheng ZHANG ; Lidian CHEN
Chinese Journal of Rehabilitation Theory and Practice 2015;21(6):642-647
Objective To explore the effects of electroacupuncture at Baihui (DU20) acupoint on learning and memory and its possible mechanism through the expression of brain-derived neurotrophic factor (BDNF) in APP/PS1 double-transgenic mice. Methods 30 female APP/PS1 double transgenic mice were randomly divided into model group, DU20 group and non-acupoint group, and 10 wild type mice con-sisted of wild group. DU20 group received electroacupuncture at Baihui and the non-acupoint group received electroacupuncture at non-acu-point for 28 days. Learning and memory was tested by Morris water maze. Deposition ofβ-amyloid (Aβ) peptide was determined by immu-nohistochemical staining. The expression of BDNF in cortex was examined by RT-PCR and Western blotting. Results Compared with the model group, DU20 group ameliorated the learning and memory ability of APP/PS1 double-transgenic mice (P<0.05), decreased the deposi-tion of Aβpeptide (P<0.05) and upregulated the gene and protein levels of BDNF (P<0.01). There was no significant difference between the model group and non-acupoint group (P>0.05). Conclusion Electroacupuncture at DU20 acupoint could ameliorate learning and memory in APP/PS1 double-transgenic mice. The mechanism may be related to increase the expression of BDNF and decrease the deposition of Aβ.
2.Effects of Shenfu yixin granule on mitochondrial autophagy of cardiomyocytes in rats with heart failure after acute yocardial infarction
Yaxuan CAO ; Rongfei ZHENG ; He WANG ; Yingjie CAO ; Wenjie DONG ; Lin CUI ; Bin LI ; Yushan CHEN ; Mingjun ZHU
China Pharmacy 2022;33(10):1183-1188
OBJECTIVE To study the effects of Shenfu yixin granule on mitochondrial autophagy of cardiomyocytes in rats with heart failure after acute myocardial infarction. METHODS The model of heart failure after acute myocardial infarction was established by ligaturing the anterior descending branch of the left coronary artery in rats. The model rats were divided into model group,Shenfu yixin granule low-dose and high-dose groups (1.76,8.8 g/kg),Fosinopril sodium tablets group (positive control ,4 mg/kg),sham operation group was set up (only threading without ligation at the same position ),with 8 rats in each group. After 4 weeks of drug intervention ,the hemodynamic indexes of rats in each group were measured by physiological recorder. The pathological changes of myocardial tissue were observed in each group. The level of oxidative stress in cardiomyocytes , mitochondrial membrane potential ,protein expression of PTEN-induced putative kinase 1(PINK1),E3 ubiquitin ligase Parkin and ubiquitin binding protein P 62 in myocardial tissue of rats in each group were detected. RESULTS Compared with sham operation group ,the pathological injuries such as myocardial fiber morphology disorder and inflammatory cell infiltration were serious. The left ventricular end systolic pressure (LVESP),maximum rate of rise of left ventricular internal pressure (+dp/dtmax), maximun rate of decrease of left ventricular internal pressure (-dp/dtmax),total antioxidant capacity ,mitochondrial membrane potential,PINK1,Parkin and P 62 protein expression were significantly decreased in model group (P<0.01). The left ventricular end diastolic pressure (LVEDP),the level of reactive oxygen species and the activity of reduced nicotinamide adenine dinucleotide phosphate in left ventricular ischemic cardiomyocytes were significantly increased (P<0.01). Compared with model group ,the pathological injuries of myocardial tissue in intervention groups were alleviated ,and above indexes were improved in varying degrees(P<0.01 or P<0.05). CONCLUSIONS Shenfu y ixin granule can reduce the level of oxidative stress and alleviate heart failure after acute myocardial infarction ,which may be related to the activation of Parkin-dependent pathway to strengthen mitochondrial autophagy and reduce mitochondrial dysfunction.