Pu-erh Tea Restored Circadian Rhythm Disruption by Regulating Tryptophan Metabolism

Abstract

Pu-erh tea is a healthy beverage rich in phytochemicals, and its effect on the risk of inducing circadian rhythm disorders (CRD) is unclear. In this study, healthy mice were given water or 0.25% (w/v) Pu-erh tea for 7 weeks, followed by a 40 day disruption of the light/dark cycle. CRD caused dysregulation of neurotransmitter secretion and clock gene oscillations, intestinal inflammation, and disruption of intestinal microbes and metabolites. Pu-erh tea boosted the indole and 5-hydroxytryptamine pathways of tryptophan metabolism via the gut–liver–brain axis. Furthermore, its metabolites (e.g., IAA, Indole, 5-HT) enhanced hepatic glycolipid metabolism and down-regulated intestinal oxidative stress by improving the brain hormone release. Tryptophan metabolites and bile acids also promoted liver lipid metabolism and inhibited intestinal inflammation (MyD88/NF-κB) via the enterohepatic circulation. Collectively, 0.25% (w/v) Pu-erh tea has the potential to prevent CRD by promoting indole and 5-HT pathways of tryptophan metabolism and signaling interactions in the gut–liver–brain axis.

Gut Microbiota-Derived Tryptophan Metabolites Maintain Gut and Systemic Homeostasis

“…Myristica fragrans regulated the gut microbes and metabolites to activate Trp metabolite-mediated AhR in mice fed a high-fat diet [ 52 ]. Pu-erh tea could boost the indole and 5-hydroxytryptamine pathways of the Trp metabolism [ 53 ]. The metabolomic analysis revealed metabolic profile alternations in response to the gut microbiota reprogrammed by a qingchang wenzhong decoction (QCWZD), especially enhanced Trp metabolism [ 54 ].…”

Long-term Pu-erh tea consumption improves blue light-induced depression-like behaviors

“…Here, we have proposed Pu-erh tea as a dietary intervention to regulate depressive behaviors, because our laboratory previously reported that 0.25% (w/v) Pu-erh tea has the potential to regulate tryptophan metabolism to reduce the risk of depression. 13 This work has demonstrated that BLAN induced depression-like behaviors which caused damage to the BBB, neuro-inflammatory response, and intestinal microbiological disorders for the first time. This evidence indicates that using electronic equipment for a long time at night increases the risk of depression.…”

“…The specific experimental method for gut microbiota analysis was reported in our previous paper. 13 Total DNA from the feces microbial community was extracted according to the kit instructions (Omega Bio-Tek, Norcross, GA, USA) and 16s rRNA was amplified by PCR (forward primer (5′-ACTCC-TACGGGAGGCAG-3′) and reverse primer (5′-GGAC-TACHVGGGTWTCTAAT-3′), gene V3-V4 region). The linear discriminant analysis effect size (LEfSe) method can be used to discover the species characteristics that best explain the differences between groups in two or more samples, and the extent to which these characteristics influence the differences between groups.…”

“…Meanwhile, Pu-erh tea could regulate tryptophan metabolism, and tryptophan can be converted to serotonin (5-hydroxytryptamine; 5-HT, an essential neurotransmitter in the central nervous system that has been proved to be associated with changes in mood, depression, or cognition). 12,13 Therefore, we speculate that long-term Pu-erh tea intake could have protective effects on depression by regulating the microbiota-gut-brain axis.…”

Selenium Antagonizes Cadmium-Induced Inflammation and Oxidative Stress via Suppressing the Interplay between NLRP3 Inflammasome and HMGB1/NF-κB Pathway in Duck Hepatocytes

“…Huang et al discovered that TLR4 could aggravate lung injury by activating the MYD88/NF-κB pathway [ 62 ]. Otherwise, it could reduce intestinal inflammation and slow down intestinal barrier damages by inhibiting the MYD88/NF-κB pathway [ 63 ]. According to our results, Cd remarkably promoted the expression level of extranuclear HMGB1, and the expression levels of the HMGB1/NF-κB pathway-related factors (HMGB1, TLR4, MYD88, NF-κB and p-65/p65) were obviously elevated, while the above changes were significantly reduced after co-treatment of Se and Cd, confirming that exposure of Cd to duck hepatocytes caused the activation of the HMGB1/NF-κB pathway, which further expanded the inflammatory response.…”