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Article Publish Status: FREE
Abstract Title:

Vitamin D3 promotes autophagy in THP-1 cells infected with.

Abstract Source:

Exp Ther Med. 2022 Mar ;23(3):240. Epub 2022 Jan 25. PMID: 35222717

Abstract Author(s):

Yiming Wu, Xue Lin, Fuyang Song, Di Xue, Yujiong Wang

Article Affiliation:

Yiming Wu

Abstract:

Tuberculosis (TB) is a major disease that causes mortality worldwide. The lethality of this disease is a result of the contagious bacteria. Infection can inhibit phagosomal maturation, withmainly attacking macrophages and inhibiting autophagy and apoptosis. Vitamin D has been used to treat tuberculosis, whereby the active metabolite, 1,25-dihydroxyvitamin D, may enhance the immune response to. Moreover, macrophages infected withhave a high demand for Ca. However, the mechanisms by which vitamin D3 protects against and treats TB remain unclear. In the present study, MTT assay showed that vitamin D3 decreased the viability of THP-1 cells in a dose- and time-dependent manner. Autophagy-related factors in THP-1 cells infected withwere analyzed by western blotting and RT-qPCR and the results demonstrated that vitamin D3 significantly increased the expression level of p62, LC3Ⅱ/LC3Ⅰ, Beclin-1, ATG-5 and AMPK in THP-1 cells followinginfection. The Caconcentration assay demonstrated that vitamin D3 may promoted cellular autophagy by inhibiting the concentration of Ca. Furthermore, the effect of vitamin D3 oninfection was also assessed using Balb/c mice; pulmonary injury was assessed by H&E staining of the lungs tissue. The results demonstrated that vitamin D3 markedly attenuated cellular damage caused byinfection. In conclusion, the present study indicated that vitamin D3 may activate cell autophagy signals by inhibiting the concentration of Ca. These data may improve understanding of the effect of vitamin D3 oninfection and help determine the underlying mechanism of vitamin D3 to alleviate and treat the inflammatory response caused by TB.

Study Type : Animal Study

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