LIU, WEIWEI
Effects of Vitamin D3 on Inflammatory Bowel Disease in Rats via the Toll-Like Receptor 4/Myeloid Differentiation Primary Response 88/Nuclear Factor Kappa Light Chain Enhancer of Activated B Cells Signaling Pathway - Vol.83(3), May-June - Mumbai Indian Journal of Pharmaceutical Science 2021 - 569-574p.
To assess the ameliorating effects of vitamin D3 on inflammatory bowel disease in rats via the Toll-like
receptor 4/myeloid differential factor 88/nuclear factor kappa B signaling pathway. Thirty two rats were
randomly assigned into Control group, model group (Vehicle group), low-concentration vitamin D3 group
(vitamin D3 low group) and high-concentration vitamin D3 group (vitamin D3 high group). The model
of inflammatory bowel disease was constructed using 3 % dextran sodium sulfate and given different
concentrations of vitamin D3. Disease activity index score was calculated, colon tissues were pathologically
scored by hematoxylin-eosin staining, and the mRNA expression levels of Toll-like receptor 4/myeloid
differential factor 88/nuclear factor kappa B were measured by quantitative reverse transcription-
polymerase chain reaction. The expression levels of serum tumor necrosis factor-α, pro-inflammatory
factors interleukin 1β and interleukin 6, as well as anti-inflammatory factor interleukin 10 were detected
through enzyme-linked immunosorbent assay. The disease activity index score, mRNA expression levels of
Toll-like receptor 4/myeloid differential factor 88/nuclear factor kappa B and expression levels of tumor
necrosis factor-α, interleukin 1β and interleukin 6 were significantly higher in Vehicle group than those
in Control group, while the expression level of interleukin-10 was lower in Vehicle group (p<0.05). After
intervention with vitamin D3, vitamin D3 low group and vitamin D3 high group had significantly decreased
disease activity index score, messenger RNA expression levels of Toll-like receptor 4/myeloid differential
factor 88/nuclear factor kappa B and expression levels of tumor necrosis factor-α, interleukin 1β and
interleukin 6, increased interleukin-10 expression level, and relieved damage of colon tissues compared
with Vehicle group (p<0.05). Vitamin D3 ameliorates intestinal injury and colonic inflammation in
inflammatory bowel disease rats by suppressing the Toll-like receptor 4/myeloid differential factor 88/
nuclear factor kappa B signaling pathway and decreasing the expression of downstream pro-inflammatory
factors.
PHARMACEUTICS
Effects of Vitamin D3 on Inflammatory Bowel Disease in Rats via the Toll-Like Receptor 4/Myeloid Differentiation Primary Response 88/Nuclear Factor Kappa Light Chain Enhancer of Activated B Cells Signaling Pathway - Vol.83(3), May-June - Mumbai Indian Journal of Pharmaceutical Science 2021 - 569-574p.
To assess the ameliorating effects of vitamin D3 on inflammatory bowel disease in rats via the Toll-like
receptor 4/myeloid differential factor 88/nuclear factor kappa B signaling pathway. Thirty two rats were
randomly assigned into Control group, model group (Vehicle group), low-concentration vitamin D3 group
(vitamin D3 low group) and high-concentration vitamin D3 group (vitamin D3 high group). The model
of inflammatory bowel disease was constructed using 3 % dextran sodium sulfate and given different
concentrations of vitamin D3. Disease activity index score was calculated, colon tissues were pathologically
scored by hematoxylin-eosin staining, and the mRNA expression levels of Toll-like receptor 4/myeloid
differential factor 88/nuclear factor kappa B were measured by quantitative reverse transcription-
polymerase chain reaction. The expression levels of serum tumor necrosis factor-α, pro-inflammatory
factors interleukin 1β and interleukin 6, as well as anti-inflammatory factor interleukin 10 were detected
through enzyme-linked immunosorbent assay. The disease activity index score, mRNA expression levels of
Toll-like receptor 4/myeloid differential factor 88/nuclear factor kappa B and expression levels of tumor
necrosis factor-α, interleukin 1β and interleukin 6 were significantly higher in Vehicle group than those
in Control group, while the expression level of interleukin-10 was lower in Vehicle group (p<0.05). After
intervention with vitamin D3, vitamin D3 low group and vitamin D3 high group had significantly decreased
disease activity index score, messenger RNA expression levels of Toll-like receptor 4/myeloid differential
factor 88/nuclear factor kappa B and expression levels of tumor necrosis factor-α, interleukin 1β and
interleukin 6, increased interleukin-10 expression level, and relieved damage of colon tissues compared
with Vehicle group (p<0.05). Vitamin D3 ameliorates intestinal injury and colonic inflammation in
inflammatory bowel disease rats by suppressing the Toll-like receptor 4/myeloid differential factor 88/
nuclear factor kappa B signaling pathway and decreasing the expression of downstream pro-inflammatory
factors.
PHARMACEUTICS