Effects of Cannabidiol on Parkinson’s Disease in a Transgenic Mouse Model by Gut-Brain Metabolic Analysis

Table 3

Focused cerebral and fecal DEMs of each paired group comparison.

DEMs set	bM	bD	fM	fD
Call-back pattern intergroup	↓Pantothenate↓Phosphocreatine↑3-methylhistidine	↑Pantothenate↑Phosphocreatine	↓Capric acid↑Gentisic acid↑Palmitic acid↑N-acetyl-l-glutamate↑Ethyl-3-hydroxybutyrate	↑Capric acid↓Gentisic acid↓Palmitic acid↓N-acetyl-l-glutamate↓Ethyl-3-hydroxybutyrate↓3-methylhistidine
Highly correlated intragroup	↑Succinate↑(R)-3-hydroxybutyric acid↓1,5-bisphosphate↓D-Mannose 1-phosphate↓Galactonic acid↓4-guanidinobutyric acid	↑L-cysteine↓Prostaglandin E2↓Palmitoyl CoA↓cis-Aconitate↓2-dehydro-3-deoxy-D-gluconate		↓L-glutamate↓1-ethylhistidine↓Betaine↓Nicotinate↓Anthranilic acid↓5-methylcytosine↓4-guanidinobutyric acid

↑ upregulated, ↓ downregulated, compared with the corresponding contrast group. bM: brain samples, group M versus C; bD: brain samples, group D versus M; fM: feces samples, group M versus C; fD: feces samples, group D versus M. The DEMs in form of bold within a certain group are highly correlated in a common regulation profile according to the KEGG pathway based clustering analysis.