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Astragaloside attenuates lipopolysaccharide‐induced cell apoptosis in human gingiva cells via MAPK signaling pathway

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AbstractSubjectsThe aim of this study was to research the antiapoptotic effect of astragaloside, the principal component of Astragalus membranaceus (Fisch) Bge, in human gingiva cells induced by lipopolysaccharide (LPS).MethodsAccording to the treatment, human gingiva cells were divided into five groups, including (1) control group without drug treatment; (2) imitating group, treated with LPS (10 μg·mL−1) alone; (3) low group, treated with LPS and 50 μmol·L −1 astragaloside; (4) medium group, treated with LPS and 100 μmol·L −1 astragaloside; and (5) high group, treated with LPS and 150 μmol·L −1 astragaloside. Cell proliferation and apoptosis were investigated using MTT assay and flow cytometry, respectively. Apoptosis and mitogen‐activated protein kinase associated proteins were determined using Western blot analysis.ResultsLPS significantly suppressed the proliferation of human gingiva cells, but astragaloside obviously attenuated this change with a dose‐dependent manner. LPS significantly promoted the apoptosis of human gingiva cells, but astragaloside treatments significantly attenuated this change with a dose‐dependent manner. In addition, LPS could significant upregulated the expression of P‐p38, P‐JNK, Bax, and caspase‐3.ConclusionAstragaloside preformed a promising antiapoptotic role in apoptosis of human gingiva cells induced by LPS. This finding might provide us with a novel therapeutic method in tooth protection.
Title: Astragaloside attenuates lipopolysaccharide‐induced cell apoptosis in human gingiva cells via MAPK signaling pathway
Description:
AbstractSubjectsThe aim of this study was to research the antiapoptotic effect of astragaloside, the principal component of Astragalus membranaceus (Fisch) Bge, in human gingiva cells induced by lipopolysaccharide (LPS).
MethodsAccording to the treatment, human gingiva cells were divided into five groups, including (1) control group without drug treatment; (2) imitating group, treated with LPS (10 μg·mL−1) alone; (3) low group, treated with LPS and 50 μmol·L −1 astragaloside; (4) medium group, treated with LPS and 100 μmol·L −1 astragaloside; and (5) high group, treated with LPS and 150 μmol·L −1 astragaloside.
Cell proliferation and apoptosis were investigated using MTT assay and flow cytometry, respectively.
Apoptosis and mitogen‐activated protein kinase associated proteins were determined using Western blot analysis.
ResultsLPS significantly suppressed the proliferation of human gingiva cells, but astragaloside obviously attenuated this change with a dose‐dependent manner.
LPS significantly promoted the apoptosis of human gingiva cells, but astragaloside treatments significantly attenuated this change with a dose‐dependent manner.
In addition, LPS could significant upregulated the expression of P‐p38, P‐JNK, Bax, and caspase‐3.
ConclusionAstragaloside preformed a promising antiapoptotic role in apoptosis of human gingiva cells induced by LPS.
This finding might provide us with a novel therapeutic method in tooth protection.

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