Post-stroke depression is a common complication after stroke,which seriously affects the quality of life and clinical prognosis of stroke patients.Acupuncture therapy for post-stroke depression has been proven effective.This article reviewed recent clinical studies on acupuncture therapy for post-stroke depression from the perspectives of pure acupuncture therapy,electroacupuncture therapy,head acupuncture therapy,auricular acupuncture therapy,and comprehensive therapy.The acupoint selection focused on the Governor Vessel,combined with the acupoints of the bladder meridian,liver meridian and pericardium meridian.The comprehensive therapy combined acupuncture with Chinese materia medica,moxibustion,music therapy and rehabilitation training is currently the main treatment approach.Further analysis on the shortcomings of the field could provide references for clinical protocols and mechanism research of acupuncture therapy for post-stroke depression.

Post-stroke depression is a common complication after stroke,which seriously affects the quality of life and clinical prognosis of stroke patients.Acupuncture therapy for post-stroke depression has been proven effective.This article reviewed recent clinical studies on acupuncture therapy for post-stroke depression from the perspectives of pure acupuncture therapy,electroacupuncture therapy,head acupuncture therapy,auricular acupuncture therapy,and comprehensive therapy.The acupoint selection focused on the Governor Vessel,combined with the acupoints of the bladder meridian,liver meridian and pericardium meridian.The comprehensive therapy combined acupuncture with Chinese materia medica,moxibustion,music therapy and rehabilitation training is currently the main treatment approach.Further analysis on the shortcomings of the field could provide references for clinical protocols and mechanism research of acupuncture therapy for post-stroke depression.

Structural and functional changes of endothelial cells are the basic pathology of many diseases. Pyroptosis is a kind of newly discovered programmed cell death which causes the formation of large pores in the membrane that drive swelling and membrane rupture. Membrane rupture disperses cytosolic contents which further elicit a systemic inflammatory response. Pyroptosis of endothelial cells make a difference in the occurrence and developement of many diseases, including Atherosclerosis, myocardial ischemia-reperfusion injury, acute lung injury, traumatic brain injury and diabetes. In this article, the progress over the years of the research on the involvement of vascular endothelial cells in the pyroptosis is reviewed.

Mutations or inactivation of parkin, an E3 ubiquitin ligase, are associated with familial form or sporadic Parkinson's disease (PD), respectively, which manifested with the selective vulnerability of neuronal cells in substantia nigra (SN) and striatum (STR) regions. However, the underlying molecular mechanism linking parkin with the etiology of PD remains elusive. Here we report that p62, a critical regulator for protein quality control, inclusion body formation, selective autophagy and diverse signaling pathways, is a new substrate of parkin. P62 levels were increased in the SN and STR regions, but not in other brain regions in parkin knockout mice. Parkin directly interacts with and ubiquitinates p62 at the K13 to promote proteasomal degradation of p62 even in the absence of ATG5. Pathogenic mutations, knockdown of parkin or mutation of p62 at K13 prevented the degradation of p62. We further showed that parkin deficiency mice have pronounced loss of tyrosine hydroxylase positive neurons and have worse performance in motor test when treated with 6-hydroxydopamine hydrochloride in aged mice. These results suggest that, in addition to their critical role in regulating autophagy, p62 are subjected to parkin mediated proteasomal degradation and implicate that the dysregulation of parkin/p62 axis may involve in the selective vulnerability of neuronal cells during the onset of PD pathogenesis.
Adaptor Proteins, Signal Transducing ; chemistry ; metabolism ; Animals ; HEK293 Cells ; Heat-Shock Proteins ; chemistry ; metabolism ; Humans ; Lysine ; metabolism ; Mice ; Neurons ; metabolism ; pathology ; Oxidopamine ; pharmacology ; Parkinson Disease ; metabolism ; pathology ; Proteasome Endopeptidase Complex ; metabolism ; Protein Stability ; Proteolysis ; drug effects ; Sequestosome-1 Protein ; Ubiquitin-Protein Ligases ; metabolism ; Ubiquitination ; drug effects