ReferenceID 5313

Geniposide ameliorated dexamethasone-induced endoplasmic reticulum stress and mitochondrial apoptosis in osteoblasts

J Ethnopharmacol

Ethnopharmacological relevance: Eucommia ulmoides Oliver has been traditionally used for treatment of various diseases, including osteoporosis, knee pain, and paralysis. The extract of Eucommia ulmoides has been reported

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Reference Id
5313
Evidence Id
21903
Core Evidence Id
21903
Source Reference Id
3877
Herb2 Reference Id
HBREF004674
Subject Paper Key
HBIN027450_35240241
Pubmed Id
35240241
Doi
10.1016/j.jep.2022.115154
Paper Title
Geniposide ameliorated dexamethasone-induced endoplasmic reticulum stress and mitochondrial apoptosis in osteoblasts
Paper Abstract
Ethnopharmacological relevance: Eucommia ulmoides Oliver has been traditionally used for treatment of various diseases, including osteoporosis, knee pain, and paralysis. The extract of Eucommia ulmoides has been reported to stimulate the bone formation and suppress the bone resorption, leading to protection against osteoporosis (OP). Geniposide (GEN) has been considered as one of the effective compounds responsible for the therapeutic efficacy of Eucommia ulmoides against OP. Aim of the study: To explore whether GEN protected against dexamethasone (DEX)-induced osteoporosis (OP) by activating NRF2 expression and inhibiting endoplasmic reticulum (ER) stress. Materials and methods: The DEX-induced rat OP models were duplicated. The pathological changes were examined by histological/immunohistochemical evaluation and micro-computed tomography (micro-CT) assessment. Apoptosis was detected by a flow cytometer. Mitochondrial Ca 2+ concentrations and mitochondrial membrane potential were detected. Western blot assays were used to detect the protein expression. Results: GEN effectively reversed DEX-induced pathological changes of trabecular bone in rats. In addition, the DEX-increased expression of ATF4/CHOP was also ameliorated. In MC3T3-E1 cells, DEX promoted endoplasmic reticulum (ER) stress and mitochondrial apoptosis. Inhibition of ER stress abolished the induction of apoptosis by DEX. Similarly, GEN significantly ameliorated DEX-induced mitochondrial apoptosis. The possible underlying mechanism might be associated with the pharmacological effects of GEN on activating the expression of NRF2 and alleviating ER stress in DEX-treated MC3T3-E1 cells. Conclusion: GEN ameliorated DEX-induced ER stress and mitochondrial apoptosis in osteoblasts.
Journal
J Ethnopharmacol
Publish Year
2022
Experiment Subject
rat; dex-treated mc3t3-e1 cells; mc3t3-e1 cells
Experiment Type
Animal Experiment
Phenotype Related
Paralysis; Eucommia Ulmoides; Osteoporosis; Knee Pain
Paper Title Cn
Paper Title En
Geniposide ameliorated dexamethasone-induced endoplasmic reticulum stress and mitochondrial apoptosis in osteoblasts
Bilingual Status
semi_complete