Previous studies have confirmed that Platycodon grandiflorus polysaccharide (PGPS) has the effects of regulating immunity and anti-apoptosis, but its effect on mitochondrial damage and apoptosis caused by PRV infection is still unclear. In this research, the effects of PGPS on the cell viability, mitochondria morphology, mitochondrial membrane potential and apoptosis caused by PRV based on PK-15 cells were respectively examined by CCK-F assay, Mito-Tracker Red CMXRos, JC-1 staining method and Western blot etc. CCK-F test results showed that PGPS had a protective effect on the decrease of cell viability caused by PRV. The results of morphological observation found that PGPS can improve mitochondrial morphology damage, mitochondrial swelling and thickening, and cristae fracture. Fluorescence staining test results showed that PGPS alleviated the decrease of mitochondrial membrane potential and apoptosis in infected cells. The expression of apoptosis-related proteins showed that PGPS down-regulated the expression of the pro-apoptotic protein Bax and up-regulated the expression of the anti-apoptotic protein Bcl-2 in infected cells. These results indicated that PGPS protected against PRV-induced PK-15 cell apoptosis by inhibiting mitochondrial damage.
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http://dx.doi.org/10.1007/s12013-023-01141-4 | DOI Listing |
PLoS One
January 2025
Department of Anesthesiology & Perioperative Medicine, University of Rochester, Rochester, New York, United States of America.
Neurodegenerative diseases are often characterized by mitochondrial dysfunction. In Alzheimer's disease, abnormal tau phosphorylation disrupts mitophagy, a quality control process through which damaged organelles are selectively removed from the mitochondrial network. The precise mechanism through which this occurs remains unclear.
View Article and Find Full Text PDFAging Dis
December 2024
Department of Sports Science, College of Natural Science, Jeonbuk National University, Jeonju 54896, Korea.
The negative effects of particulate matter up to 2.5 μm in diameter (PM) and their mediating mechanisms have been studied in various tissues. However, little is known about the mechanism and long-term tracking underlying the sex-dependent effects of PM on skeletal muscle system modulation.
View Article and Find Full Text PDFAging Dis
December 2024
School of Athletic Performance, Shanghai University of Sport, Shanghai, China.
Skeletal muscle dysfunction (SMD), one of the extrapulmonary complications in patients with chronic obstructive pulmonary disease (COPD), considerably influences patient prognosis. Mitochondria regulates their dynamic networks through a mitochondria quality control (MQC) mechanism, involving mitochondrial biogenesis, mitochondrial dynamics, and mitophagy. The MQC is crucial for mitochondrial homeostasis and health, and disruption of it can lead to mitochondrial damage, which is a key factor in the structural and functional impairment of skeletal muscle in COPD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Background: Brain endothelial cell (EC) stress, including that induced by vascular amyloid β (Aβ) deposits in cerebral amyloid angiopathy (CAA) and Alzheimer's disease (AD), contributes to cerebral blood flow impairment, blood brain barrier (BBB) damage, neurovascular unit dysfunction, microhemorrhages and hypoperfusion, precipitating neurodegeneration and neuroinflammation processes. Epidemiological and experimental evidence suggests that hyperhomocysteinemia (Hhcy) contributes to increasing AD risk as well as CAA pathology. However, the cellular and molecular mechanisms through which Aβ and Hhcy drive EC and BBB dysfunction, whether the molecular effects of these challenges are additive or independent, and possible therapeutic strategies, remain to be determined.
View Article and Find Full Text PDFBackground: Directed by the enzyme pair PINK1 and PRKN, mitophagy is a crucial mitochondrial quality control mechanism that selectively decorates damaged mitochondria with phosphorylated ubiquitin (pS65-Ub), facilitating their lysosomal degradation. The dynamic pS65-Ub signal accumulates upon enhanced activation from increased mitochondrial damage or upon reduced autophagic-lysosomal flux. Previous studies including ours demonstrated altered mitophagy and elevated pS65-Ub levels in Parkinson's and Alzheimer's disease brains that also independently associated with α-synuclein, tau, or amyloid pathology.
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