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| http://dx.doi.org/10.1016/j.jpha.2023.10.003 | DOI Listing |
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Effects and mechanism of combination of Platycodon grandiflorum polysaccharides and Platycodon saponins in the treatment of chronic obstructive pulmonary disease rats through the gut-lung axis.
J Ethnopharmacol
December 2024
College of pharmacy, Anhui University of Chinese Medicine, Hefei 230012, Anhui, China; MOE-Anhui Joint Collaborative Innovation Center for Quality Improvement of Anhui Genuine Chinese Medicinal Materials,Hefei 230012, Anhui, China; Anhui Province Key Laboratory of Pharmaceutical Preparation Technology and Application, Hefei, Anhui, 230012, China. Electronic address:
Ethnopharmacological Relevance: Platycodon grandiflorum (Jacq.) A. DC.
View Article and Find Full Text PDFPlatycodin D2 Mediates Incomplete Autophagy and Ferroptosis in Breast Cancer Cells by Regulating Mitochondrial ROS.
Phytother Res
November 2024
Key Laboratory of Jilin Province for Traditional Chinese Medicine Prevention and Treatment of Infectious Diseases, College of Integrative Medicine, Changchun University of Chinese Medicine, Changchun, P. R. China.
Article Synopsis
- Platycodin D2 (PD2), a natural compound from the root of Platycodon grandiflorum, has shown potential benefits in anti-inflammatory, antioxidative, antitumor, and immune-boosting properties but its effects on breast cancer cells were previously unexplored.
- The study revealed that PD2 induces mitochondrial damage and increases reactive oxygen species (mtROS), leading to the inhibition of autophagy and ferroptosis, both of which contribute to reduced breast cancer cell proliferation.
- Overall, PD2 demonstrates promising results as a potential treatment strategy for breast cancer by promoting specific cellular processes that inhibit tumor growth.
Platycodin D reduces PD-L1 levels by inhibiting LXR-β activity and combines with nintedanib to enhance the tumor-killing effect of T cells.
FEBS Lett
December 2024
ECUST-FONOW Joint Research Center for Innovative Medicines, East China University of Science and Technology, Shanghai, China.
Article Synopsis
- - Most tumors resist treatment with PD-1/PD-L1 inhibitors due to low levels of MHC-I, which affects how tumor cells present antigens to the immune system.
- - Three plant-derived compounds, platycodin D (PD), polygalacin D, and platycodin D2, were found to significantly lower PD-L1 levels by interacting with liver X receptor β (LXR-β).
- - Combining PD with nintedanib, a drug that boosts MHC-I expression, improved the ability of T cells to recognize and destroy tumors, shedding light on new treatment strategies.
Platycodin D ameliorates polycystic ovary syndrome-induced ovarian damage by upregulating CD44 to attenuate ferroptosis.
Free Radic Biol Med
November 2024
Reproductive Medical Center, Renmin Hospital of Wuhan University, Wuhan, China; Hubei Clinic Research Center for Assisted Reproductive Technology and Embryonic Development, Wuhan, China. Electronic address:
Recently, the potential association between polycystic ovary syndrome (PCOS) development and progression and ferroptosis has garnered attention. Increasing evidence suggests that targeting ferroptosis may be an effective strategy for treating PCOS. First, we observed that the expression of the ferroptosis regulatory molecules SLC7A11, GPX4, and FTH1 was decreased in the granulosa cells (GCs) of patients with PCOS and ovarian tissues of rats with PCOS; in contrast, TFR1 expression was increased.
View Article and Find Full Text PDFPlatycodon D reduces obesity and non-alcoholic fatty liver disease induced by a high-fat diet through inhibiting intestinal fat absorption.
Front Pharmacol
July 2024
The Affiliated Panyu Central Hospital, Guangzhou Medical University, Guangzhou, China.
Background: Platycodin D (PD) has been reported to treat metabolic diseases, including non-alcoholic fatty liver disease. In addition, platycodin D has been reported to activate intestinal 5'AMP-activated protein kinase (AMPK) phosphorylation levels, thereby reducing lipid absorption. Therefore, the aim of this study is to explore whether PD activation of intestinal AMPK and reduced lipid absorption can improve non-alcoholic fatty liver disease.
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