• Title/Summary/Keyword: Pharmacological effects

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Analysis of Physical Status on COVID-19: Based on Impacts of Physical Activity (COVID-19에 대한 운동중재효과 분석)

  • Kim, Kwi-Baek;Kwak, Yi Sub
    • Journal of Life Science
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    • v.31 no.6
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    • pp.603-608
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    • 2021
  • The purpose of this perspective research is to discuss the potential role of exercise-interventions in COVID-19, terms of prevention and prognosis in the periods of the COVID-19 vaccine. SARCO-CoV-2. COVID-19 was detected as a new virus causing severe cardiovascular and respiratory complications. It emerged as a global public health emergency and national pandemic. It caused more than 1 million deaths in the first 6 months of the pandemic and resulted in huge social and economic fluctuations internationally. Unprecedented stressful situations, such as COVID-19 blue and COVID-19 red impact on many health problems. In healthy individuals, COVID-19 infection may induced no symptoms (i.e., asymptomatic), whereas others may experience flu-like symptoms, such as ARDS, pneumonia, and death. Poor health status, such as obesity and cardiovascular and respiratory complications, are high risk factors for COVID-19 prevention, occurrence, and prognosis. Several COVID-19 vaccines are currently in human trials. However, the efficacy and safety of COVID-19 vaccines, including potential side effects, such as anaphylaxis (a life-threatening allergic reaction) and rare blood clots, still need to be investigated. On the basis of direct and indirect evidence, it seems that regular and moderate physical exercise can be recommended as a nonpharmacological, efficient, and safe way to cope with COVID-19. Physical inactivity and metabolic abnormalities are directly associated with reduced immune responses, including reduced innate, CMI, and AMI responses. Due to prolonged viral shedding, quarantine in inactive, obese and disease people should likely be longer than physical active people. Multicomponent and systemic exercise should be considered for the obese, disease, and elderly people. More mechanism research is needed in this area.

Ginsenoside compound K protects against cerebral ischemia/ reperfusion injury via Mul1/Mfn2-mediated mitochondrial dynamics and bioenergy

  • Qingxia Huang;Jing Li;Jinjin Chen;Zepeng Zhang;Peng Xu;Hongyu Qi;Zhaoqiang Chen;Jiaqi Liu;Jing Lu;Mengqi Shi;Yibin Zhang;Ying Ma;Daqing Zhao;Xiangyan Li
    • Journal of Ginseng Research
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    • v.47 no.3
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    • pp.408-419
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    • 2023
  • Background: Ginsenoside compound K (CK), the main active metabolite in Panax ginseng, has shown good safety and bioavailability in clinical trials and exerts neuroprotective effects in cerebral ischemic stroke. However, its potential role in the prevention of cerebral ischemia/reperfusion (I/R) injury remains unclear. Our study aimed to investigate the molecular mechanism of ginsenoside CK against cerebral I/R injury. Methods: We used a combination of in vitro and in vivo models, including oxygen and glucose deprivation/reperfusion induced PC12 cell model and middle cerebral artery occlusion/reperfusion induced rat model, to mimic I/R injury. Intracellular oxygen consumption and extracellular acidification rate were analyzed by Seahorse multifunctional energy metabolism system; ATP production was detected by luciferase method. The number and size of mitochondria were analyzed by transmission electron microscopy and MitoTracker probe combined with confocal laser microscopy. The potential mechanisms of ginsenoside CK on mitochondrial dynamics and bioenergy were evaluated by RNA interference, pharmacological antagonism combined with co-immunoprecipitation analysis and phenotypic analysis. Results: Ginsenoside CK pretreatment could attenuate mitochondrial translocation of DRP1, mitophagy, mitochondrial apoptosis, and neuronal bioenergy imbalance against cerebral I/R injury in both in vitro and in vivo models. Our data also confirmed that ginsenoside CK administration could reduce the binding affinity of Mul1 and Mfn2 to inhibit the ubiquitination and degradation of Mfn2, thereby elevating the protein level of Mfn2 in cerebral I/R injury. Conclusion: These data provide evidence that ginsenoside CK may be a promising therapeutic agent against cerebral I/R injury via Mul1/Mfn2 mediated mitochondrial dynamics and bioenergy.