Oxygen is a necessary substance for life activities, but reduced oxygen utilization due to high altitude exposure and respiratory dysfunction diseases could lead to pathological changes in the organisms. Herein gypenosides, the active ingredients in the food and medicine resource plant Gynostemma pentaphyllum (Thunb.) Makino were found to alleviate hypoxia-induced injury in PC12 cells. Moreover, hypoxia induced an increase in Ca and reactive oxygen species content, and such patterns were both significantly reduced by gypenosides treatment. At the same time, gypenosides significantly blocked the decrease of both NO content and mitochondrial membrane potential caused by hypoxia. Furthermore, gypenosides gavage treatment significantly prolonged the survival time of C57BL/6 mice in confinement up to 24.3% and enhanced the locomotor ability of mice. Therefore, gypenosides have good neuroprotective effects and hypoxia tolerance activity and have the prospect of being developed as a preventive and therapeutic drug for hypoxia-related diseases. PRACTICAL APPLICATIONS: Gypenosides can enhance tolerance of cells and mice to hypoxia and have the potential to be developed into hypoxia-resistant health food and drugs.
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http://dx.doi.org/10.1111/jfbc.14448 | DOI Listing |
Sci Rep
January 2025
Department of Pathology, Dokkyo Medical University School of Medicine and Graduate School of Medicine, 880 Kitakobayashi, Mibu, Shimotsugagun, Tochigi, 321-0293, Japan.
Although alveolar hyperoxia exacerbates lung injury, clinical studies have failed to demonstrate the beneficial effects of lowering the fraction of inspired oxygen (FO) in patients with acute respiratory distress syndrome (ARDS). Atelectasis, which is commonly observed in ARDS, not only leads to hypoxemia but also contributes to lung injury through hypoxia-induced alveolar tissue inflammation. Therefore, it is possible that excessively low FO may enhance hypoxia-induced inflammation in atelectasis, and raising FO to an appropriate level may be a reasonable strategy for its mitigation.
View Article and Find Full Text PDFInflamm Res
January 2025
Department of Anesthesiology, Critical Care, and Surgery, Duke University School of Medicine, Durham, NC, USA.
Background: Mitochondria generate the adenosine triphosphate (ATP) necessary for eukaryotic cells, serving as their primary energy suppliers, and contribute to host defense by producing reactive oxygen species. In many critical illnesses, including sepsis, major trauma, and heatstroke, the vicious cycle between activated coagulation and inflammation results in tissue hypoxia-induced mitochondrial dysfunction, and impaired mitochondrial function contributes to thromboinflammation and cell death.
Methods: A computer-based online search was performed using the PubMed and Web of Science databases for published articles concerning sepsis, trauma, critical illnesses, cell death, mitochondria, inflammation, coagulopathy, and organ dysfunction.
Biomed Chromatogr
February 2025
School of Pharmaceutical Sciences, Jilin University, Changchun, People's Republic of China.
Previous studies have suggested that ginsenoside Rg glycine ester derivative (RG) exhibits therapeutic potential in mitigating hypoxia. This study aimed to elucidate the potential mechanism of RG in hypoxia injury through a combined approach of metabolomics and network pharmacology. Initially, a CoCl-induced cell hypoxia model was established, and the therapeutic impact of RG on biochemical indices was evaluated.
View Article and Find Full Text PDFChronic exposure to high altitudes causes pathophysiological cardiac changes that are characterized by cardiac dysfunction, cardiac hypertrophy, and decreased energy reserves. However, finding specific pharmacological interventions for these pathophysiological changes is challenging. In this study, we identified tetramethylpyrazine (TMP) as a promising drug candidate for cardiac dysfunction caused by simulated high-altitude exposure.
View Article and Find Full Text PDFZhong Nan Da Xue Xue Bao Yi Xue Ban
August 2024
Department of Radiology, Third Xiangya Hospital, Central South University, Changsha 410013, China.
Objectives: Islet transplantation is one of the most promising curative methods for type 1 diabetes mellitus (T1DM), but early hypoxic death of the graft post-transplantation impedes successful treatment. To improve the efficacy of islet transplantation and enhance islet cell resistance to hypoxia, reducing hypoxic injury before revascularization is crucial. Mesenchymal stem cells (MSCs) are known to regulate immune responses and protect against hypoxic damage through paracrine mechanisms.
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