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Questions and Answers
What is the purpose of CCK-8 solution in the experiment?
Which staining method is employed for detecting lipid droplets in the study?
Which step is performed after blocking with goat serum during the immunofluorescence staining procedure?
What is the magnification of the fluorescence microscope used for imaging?
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What method is used to analyze gut microbiota changes in the study?
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What role does VD play in relation to HFD-induced hepatic injury?
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Which of the following components does pyroptosis involve?
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How does GSDMD-N fragment overexpression affect the protective effects of VD?
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What was observed regarding gut microbiota due to VD treatment?
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What is one consequence of NAFLD as mentioned in the content?
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Study Notes
Vitamin D and NAFLD
- Vitamin D (VD) attenuated hepatic injury and lipid accumulation, reduced NLRP3 inflammasome activation and pyroptosis both in vivo (mice) and in vitro (BRL-3A cells).
- GSDMD-N fragment overexpression suppressed the protective effect of VD on cell viability and lipid accumulation.
- VD restored gut microbiota dysbiosis by increasing the relative abundance of Lactobacillus and reducing that of Acetatifactor, Oscillibacter and Flavonifractor.
NAFLD
- Non-alcoholic fatty liver disease (NAFLD) is a spectrum of liver conditions from fatty liver to cirrhosis and even hepatocellular carcinoma.
- NAFLD affects 25% of the adult population globally.
Pyroptosis
- Pyroptosis is an inflammatory form of programmed cell death.
- The canonical pathway is initiated by inflammasomes, which activate caspase-1.
- Caspase-1 cleaves pro-IL-1β and pro-IL-18 into their active forms (mature IL-1β and IL-18).
- Caspase-1 also cleaves gasdermin D (GSDMD) into a N-terminal and C-terminal fragment.
Gut Microbiota
- HFD consumption significantly decreased the relative abundance of Bacteroidetes while VD administration significantly decreased the relative abundance of Firmicutes and increased the relative abundance of Bacteroidetes.
- VD effectively relieved HFD-induced gut microbiota dysbiosis.
Experiment Results
- In vivo: VD administration restored the HFD-triggered production of fat vacuoles and disordered structure of hepatic lobules.
- In vitro: VD significantly decreased the expression of NLRP3, ASC, pro-caspase-1, cleaved-caspase-1, pro-IL-1β, IL-1β and GSDMD-N in BRL-3A cells.
- VD significantly decreased TG content and lipid accumulation in BRL-3A cells.
- GSDMD-N fragment overexpression reversed the VD-induced decreases in the expression of GSDMD-N, NLRP3, ASC, cleaved-caspase-1, pro-IL-1β, IL-1β and GSDMD-N, indicating that VD might attenuate NAFLD through inhibiting pyroptosis.
- GSDMD-N fragment overexpression significantly reversed the VD-induced decreases in loss of cell viability, indicating that VD promoted the viability of the BRL-3A cells stimulated by PA and LPS via the regulation of pyroptosis.
- GSDMD-N fragment overexpression significantly reversed the VD-induced reduction in TG contents and accumulation of lipid droplets.
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Description
Test your knowledge on the relationship between Vitamin D and Non-Alcoholic Fatty Liver Disease (NAFLD). This quiz will cover the effects of Vitamin D on hepatic injury, lipid accumulation, and the mechanisms of pyroptosis in the context of NAFLD. Explore how gut microbiota plays a role in these processes as well.
