1. Epigallocatechin gallate protects MC3T3-E1 cells from cadmium-induced apoptosis and dysfunction via modulating PI3K/AKT/mTOR and Nrf2/HO-1 pathways.
- Author
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Wei F, Lin K, Ruan B, Wang C, Yang L, Wang H, and Wang Y
- Subjects
- Animals, Mice, Cadmium toxicity, Cell Differentiation drug effects, Cell Line, Membrane Proteins, Catechin analogs & derivatives, Catechin pharmacology, Apoptosis drug effects, NF-E2-Related Factor 2 metabolism, TOR Serine-Threonine Kinases metabolism, Signal Transduction drug effects, Heme Oxygenase-1 metabolism, Proto-Oncogene Proteins c-akt metabolism, Phosphatidylinositol 3-Kinases metabolism, Osteoblasts drug effects, Osteoblasts metabolism
- Abstract
Epigallocatechin gallate (EGCG), an active constituent of tea, is recognized for its anticancer and anti-inflammatory properties. However, the specific mechanism by which EGCG protects osteoblasts from cadmium-induced damage remains incompletely understood. Here, the action of EGCG was investigated by exposing MC3T3-E1 osteoblasts to EGCG and CdCl
2 and examining their growth, apoptosis, and differentiation. It was found that EGCG promoted the viability of cadmium-exposed MC3T3-E1 cells, mitigated apoptosis, and promoted both maturation and mineralization. Additionally, CdCl2 has been reported to inhibit both the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) and nuclear factor erythroid 2-related factor 2/heme oxygenase-1(Nrf2/HO-1) signaling pathways. EGCG treatment attenuated cadmium-induced apoptosis in osteoblasts and restored their function by upregulating both signaling pathways. The findings provide compelling evidence for EGCG's role in attenuating cadmium-induced osteoblast apoptosis and dysfunction through activating the PI3K/AKT/mTOR and Nrf2/HO-1 pathways. This suggests the potential of using EGCG for treating cadmium-induced osteoblast dysfunction., Competing Interests: The authors declare there are no competing interests., (©2024 Wei et al.)- Published
- 2024
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