Background::
Calebin-A is a minor phytoconstituent of turmeric known for its activity
against inflammation, oxidative stress, cancerous, and metabolic disorders like Non-alcoholic fatty
liver disease(NAFLD). Based on bioinformatic tools, the present study explored the intersection
of possible targets that interacted with Calebin-A and the essential genes involved in NAFLD.
Subsequently, the details of the interaction of critical proteins with Calebin-A were investigated
using the molecular docking technique.
Methods::
We first probed the intersection of genes/ proteins between NAFLD and Calebin-A
through online databases. Besides, we performed an enrichment analysis using the ClueGO plugin
to investigate signaling pathways and gene ontology. Next, we evaluate the possible interaction of
Calebin-A with significant hub proteins involved in NAFLD through a molecular docking study.
Results::
We identified 87 intersection genes Calebin-A targets associated with NAFLD. PPI network
analysis introduced 10 hub genes (TP53, TNF, STAT3, HSP90AA1, PTGS2, HDAC6,
ABCB1, CCT2, NR1I2, and GUSB). In KEGG enrichment, most were associated with Sphingolipid,
vascular endothelial growth factor A (VEGFA), C-type lectin receptor, and mitogen-activated
protein kinase (MAPK) signaling pathways. The biological processes described in 87 intersection
genes are mostly concerned with regulating the apoptotic process, cytokine production,
and intracellular signal transduction. Molecular docking results also directed that Calebin-A had a
high affinity to bind hub proteins linked to NAFLD.
Conclusion::
Here, we showed that Calebin-A, through its effect on several critical genes/ proteins
and pathways, might repress the progression of NAFLD.