Background:
Many studies have suggested that tea has antidepressant effects; however,
the underlying mechanism is not fully studied. As the main anti-inflammatory polyphenol in
tea, catechin may contribute to the protective role of tea against depression.
background:
Many studies have suggested that tea has antidepressant effects; however, the underlying mechanism is not fully studied. As the main anti-inflammatory polyphenol in tea, catechin may contribute to the protective role of tea against depression.
Objective:
The objective of this study is to prove that catechin can protect against
lipopolysaccharide (LPS)-induced depressive-like behaviours in mice, and then explore the underlying
molecular mechanisms.
objective:
The objective of this study is to prove that catechin can protect against lipopolysaccharide (LPS)-induced depressive-like behaviours in mice, and then explore the underlying molecular mechanisms.
Method:
Thirty-one C57BL/6J mice were categorized into the normal saline (NS) group, LPS
group, catechin group, and amitriptyline group according to their treatments. Elevated Plus Maze
(EPM), Tail Suspension Test (TST), and Open Field Test (OFT) were employed to assess depressive-
like behaviours in mice. RNA sequencing (RNA-seq) and subsequent Bioinformatics analyses,
such as differential gene analysis and functional enrichment, were performed on the four
mouse groups.
method:
Thirty-one C57BL/6J mice were categorized into normal saline (NS) group, LPS group, catechin group, and amitriptyline group according to their treatments. Elevated Plus Maze (EPM), Tail Suspension Test (TST), and Open Field Test (OFT) were employed to assess depressive-like behaviours in mice. RNA sequencing (RNA-seq) and subsequent Bioinformatics analyses, such as differential gene analysis and functional enrichment, were performed on the four mouse groups.
Results:
In TST, the mice in the LPS group exhibited significantly longer immobility time than
those in the other three groups, while the immobility times for the other three groups were not significantly
different. Similarly in EPM, LPS-treated mice exhibited a significantly lower percentage
in the time/path of entering open arms than the mice in the other three groups, while the percentages
of the mice in the other three groups were not significantly different. In OFT, LPS-treated
mice exhibited significantly lower percentages in the time/path of entering the centre area than
those in the other three groups. The results suggested that the LPS-induced depression models
were established successfully and catechin can reverse (LPS)-induced depressive-like behaviours
in mice. Finally, RNA-seq analyses revealed 57 differential expressed genes (DEGs) between LPS
and NS with 19 up-regulated and 38 down-regulated. Among them, 13 genes were overlapped
with the DEGs between LPS and cetechin (in opposite directions), with an overlapping p-value <
0.001. The 13 genes included Rnu7, Lcn2, C4b, Saa3, Pglyrp1, Gpx3, Lyz2, S100a8, S100a9,
Tmem254b, Gm14288, Hbb-bt, and Tmem254c, which might play key roles in the protection of
catechin against LPS-induced depressive-like behaviours in mice. The 13 genes were significantly
enriched in defense response and inflammatory response, indicating that catechin might work
through counteracting changes in the immune system induced by LPS.
Conclusion:
Catechin can protect mice from LPS-induced depressive-like behaviours through affecting
inflammatory pathways and neuron-associated gene ontologies.