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Actein alleviates 2,3,7,8-tetrachlorodibenzo-p-dioxin-mediated cellular dysfunction in osteoblastic MC3T3-E1 cells
Eun Mi Choi1, Kwang Sik Suh1, Woon-Won Jung2
1Department of Endocrinology & Metabolism, School of Medicine, Kyung Hee University, Seoul, 02447, Republic of Korea.
Environmental Toxicology
|August 25, 2017
Summary
Actein from black cohosh protects osteoblastic cells from the environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Actein mitigates TCDD-induced cell damage, oxidative stress, and promotes osteoblast differentiation.
Area of Science:
- Biochemistry
- Toxicology
- Cell Biology
Background:
- The environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is known to negatively impact bone metabolism.
- Osteoblastic cells are crucial for bone formation and are susceptible to toxic insults.
Purpose of the Study:
- To evaluate the protective effects of actein, a triterpene glycoside from black cohosh, against TCDD-induced toxicity in MC3T3-E1 osteoblastic cells.
- To elucidate the molecular mechanisms underlying actein's cytoprotective action.
Main Methods:
- MC3T3-E1 osteoblastic cells were treated with TCDD and/or actein.
- Cell viability, apoptosis, autophagy, intracellular calcium, mitochondrial membrane potential, reactive oxygen species (ROS), and cardiolipin peroxidation were assessed.
- Levels of key proteins (ERK, aryl hydrocarbon receptor, aryl hydrocarbon receptor repressor, cytochrome P450 1A1) and mRNA (superoxide dismutase, ERK1, nuclear factor kappa B) were analyzed.
- Osteoblastic differentiation markers (ALP activity, collagen content, gene expression) were evaluated.
Main Results:
- TCDD significantly reduced cell viability, increased apoptosis and autophagy, and elevated intracellular calcium, mitochondrial dysfunction, ROS production, and cardiolipin peroxidation.
- Actein pretreatment significantly mitigated TCDD-induced toxicity, including oxidative stress markers.
- Actein inhibited TCDD's effects on ERK, aryl hydrocarbon receptor, aryl hydrocarbon receptor repressor, and cytochrome P450 1A1.
- Actein restored superoxide dismutase, ERK1, and nuclear factor kappa B mRNA levels.
- Actein enhanced alkaline phosphatase activity, collagen content, and expression of osteoblastic differentiation genes.
Conclusions:
- Actein exhibits significant cytoprotective effects against TCDD-induced oxidative stress and damage in osteoblastic cells.
- Actein mitigates TCDD toxicity by modulating key signaling pathways and restoring cellular homeostasis.
- Actein promotes osteoblastic differentiation, suggesting potential therapeutic applications in bone health.
