Study on the relationship between relieving energy crisis in myofascial trigger points with An-Pressing manipulation and AMPK/PGC-1α pathway activation / 针灸推拿医学（英文版）

Objective: To explore the mechanism of An-Pressing manipulation in relieving energy crisis in chronic myofascial trigger points (MTrPs) by observing the effects of An-Pressing manipulation on adenosine triphosphate (ATP), adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) pathway and mitochondrial ultrastructure of skeletal muscle cells in MTrPs rats. Methods: Forty-eight male Sprague-Dawley rats were randomly divided into a blank group, a model group, a lidocaine group, and an An-Pressing manipulation group, with 12 rats in each group. The model group, lidocaine group and An-Pressing manipulation group were used to replicate the MTrPs rat model by blunt shock and centrifugal motion method. After modeling, the An-Pressing manipulation group was subjected to 7 times An-Pressing manipulation, once every other day; the lidocaine group was treated with 3 times of injection of lidocaine at the MTrPs, once every 6 d. The blank group and the model group were fed normally without intervention. After the intervention, local muscle tissue was taken to detect the content of ATP and the expression of AMPK, phosphorylated AMPK (phospho-AMPK), PGC-1α, and glucose transporter 4 (GluT4), and the ultrastructure of mitochondria was observed under an electron microscope. Results: Compared with the blank group, the ATP content in the model group was decreased (P<0.05), the protein expression levels of phospho-AMPK, PGC-1α, and GluT4 and the ratio of phospho-AMPK to AMPK were decreased (P<0.05); under the electron microscope, the number of mitochondria decreased, and they were deformed, small in volume, and had deformed cristae. Compared with the model group, the ATP contents in the An-Pressing manipulation group and the lidocaine group were increased (P<0.05), and the protein expression levels of phospho-AMPK, PGC-1α, and GluT4 and the ratio of phospho-AMPK to AMPK were increased (P<0.05); under the electron microscope, the number of mitochondria increased, the shape and size of the mitochondria were basically normal, and the cristae could be seen. Compared with the lidocaine group, phospho-AMPK and the ratio of phospho-AMPK to AMPK in the An-Pressing manipulation group were increased (P<0.05); under the electron microscope, the numbers of mitochondria were similar, and the shape and size of the mitochondria were basically normal without swelling, and the cristae could be observed. Conclusion: An-Pressing manipulation can increase the ATP content in MTrPs tissue, improve the expression levels of PGC-1α and GluT4 proteins and the ratio of phospho-AMPK to AMPK; its mechanism may relate to the activation of AMPK/PGC-1α signaling pathway to promote the repair of mitochondrial damages.

Effects of PGC1 / 中南大学学报(医学版)

OBJECTIVES@#Peroxisome proliferator-activated receptor gamma coactivator 1α (PGC1α) controls mitochondrial biogenesis, but its role in cardiovascular diseases is unclear. The purpose of this study is to explore the effect of PGC1α on myocardial ischemia-reperfusion injury and the underlying mechanisms.@*METHODS@#The transverse coronary artery of SD rat was ligated for 30 minutes followed by 2 hours of reperfusion. Triphenyltetrazolium chloride (TTC) staining was performed to measure the area of myocardial infarction. Immunohistochemistry and Western blotting were used to detect the PGC1α expression in myocardium. The rat cardiomyocyte H9C2 was subjected to hypoxia/reoxygenation (H/R) with the knockdown of PGC1α or hypoxia- inducible factor 1α (HIF-1α), or with treatment of metformin. Western blotting was used to detect the expression of PGC1α, HIF-1α, p21, BAX, and caspase-3. CCK-8 was performed to detect cell viability, and flow cytometry was used to detect apoptosis and mitochondrial superoxide (mitoSOX) release. RT-qPCR was used to detect the mRNA expression of PGC1α and HIF-1α. Besides, chromatin immunoprecipitation (ChIP)-qPCR and luciferase reporter gene assay were applied to detect the transcriptional regulation effect of HIF-1α on PGC1α.@*RESULTS@#After I/R, the PGC1α expression was increased in infarcted myocardium. H/R induced H9C2 cell apoptosis (@*CONCLUSIONS@#After I/R, HIF-1α up-regulates the expression of PGC1α, leading to an increase in ROS production and aggravation of injury. Metformin can inhibit the accumulation of HIF-1α during hypoxia and effectively protect myocardium from ischemia/reperfusion injury.

Role of RIP140 and PGC-1αin angiotensin Ⅱ mediated energy metabolism in cardiomyocytes / 中国药理学通报

Aim To investigate the role of transcrip-tional cofactors receptor interacting protein 140 ( RIP140 ) and peroxisome proliferator-activated recep-tor γ coactivator-1α ( PGC-1α) in the angiotensin Ⅱ( AngⅡ) mediated energy metabolism regulation in cardiomyocytes. Methods RIP140 or PGC-1α was overexpressed via adenovirus vector system. ATP con-tents were detected by luminescence detection assay system. Real-time PCR and Western blot analysis were used to measure the expressions of RIP140 and PGC-1α genes. Results After treated with 100 nmol·L-1 AngⅡfor 36h in neonatal cardiomyocytes, the content of mitochondrial ATP was reduced notably ( P <0. 01). Accordingly, the mRNA and protein levels for RIP140 were increased. However, the mRNA and pro-tein levels of PGC-1α were downregulated markedly. What’ s more,the reduction of ATP induced by AngⅡwas further aggravated by RIP 1 4 0 overexpression , but ameliorated by overexpressing PGC-1α. Conclusion The reduction of ATP mediated by AngⅡis associated with the upregulation of RIP140 , as well as the down-regulation of PGC-1α.