ArticleBMC complementary medicine and therapies2024
Ganoderma spore lipid ameliorates docetaxel, cisplatin, and 5-fluorouracil chemotherapy-induced damage to bone marrow mesenchymal stem cells and hematopoiesis.
Article in BMC complementary medicine and therapies, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Skin Aging: From Molecular Mechanisms to Therapeutic and Technological Innovations.Journal of cellular and molecular medicine · 2026Review
- Integrating Traditional Chinese Medicine and Nanotechnology for Enhanced Management of Anti-Tumor Drug Toxicity.Molecules (Basel, Switzerland) · 2026Review
- Multicomponent Ganoderma lucidum spore-based solid self-nanoemulsifying system of paclitaxel for improved lymphatic absorption and immune synergistic antitumor strategy.Journal of nanobiotechnology · 2026Article
- Human umbilical cord mesenchymal stem cells improve bone marrow hematopoiesis through regulation of bone marrow adipose tissue.Molecular and cellular biochemistry · 2025Article
- Bone-protective effects of deer-hide gelatin in cyclophosphamide-induced osteoporosis rats.Frontiers in pharmacology · 2025Article
- Ganoderma Spore Lipids Inhibit Perineural Invasion in Pancreatic Cancer by Downregulating NGF-TrkA Pathway.Journal of evidence-based integrative medicineArticle
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Abstract
backgroundA triplet chemotherapy regimen of docetaxel, cisplatin, and 5-fluorouracil (TPF) is used to treat head and neck squamous cell carcinoma; however, it is toxic to bone marrow mesenchymal stem cells (BMSCs). We previously demonstrated that Ganoderma spore lipid (GSL) protect BMSCs against cyclophosphamide toxicity. In this study, we investigated the protective effects of GSL against TPF-induced BMSCs and hematopoietic damage.
methodsBMSCs and C57BL/6 mice were divided into control, TPF, co-treatment (simultaneously treated with GSL and TPF for 2 days), and pre-treatment (treated with GSL for 7 days before 2 days of TPF treatment) groups. In vitro, morphology, phenotype, proliferation, senescence, apoptosis, reactive oxygen species (ROS), and differentiation of BMSCs were evaluated. In vivo, peripheral platelets (PLTs) and white blood cells (WBCs) from mouse venous blood were quantified. Bone marrow cells were isolated for hematopoietic colony-forming examination.
resultsIn vitro, GSL significantly alleviated TPF-induced damage to BMSCs compared with the TPF group, recovering their morphology, phenotype, proliferation, and differentiation capacity (p < 0.05). Annexin V/PI and senescence-associated β-galactosidase staining showed that GSL inhibited apoptosis and delayed senescence in TPF-treated BMSCs (p < 0.05). GSL downregulated the expression of caspase-3 and reduced ROS formation (p < 0.05). In vivo, GSL restored the number of peripheral PLTs and WBCs and protected the colony-forming capacity of bone marrow cells (p < 0.05).
conclusionsGSL efficiently protected BMSCs from damage caused by TPF and recovered hematopoiesis.
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