Yunnan Black Tea Flavonoids Can Improve Cognitive Dysfunction in Septic Mice by Activating SIRT1.

Chao Mai,Li Qiu,Yiping He,Yong Zeng,Talha Bin Emran

doi:10.1155/2021/5775040

Abstract

This study explored the effect and mechanism of Yunnan black tea flavonoids (YBTF) on cognitive dysfunction in septic mice. The mice were induced sepsis, the serum was determined using kits, and the tissue was determined by qPCR assay. The Yunnan black tea flavonoids were checked using HPLC. The test results showed that compared with the model group, YBTF could increase the survival rate of the mice; meanwhile, YBTF could also increase the total distance travelled, number of stands, and number of groomings, as well as the number of times crossing the area in the target quadrant. Detection of nerve cells showed that YBTF could reduce the rate of nerve cell apoptosis caused by sepsis. YBTF also reduced the levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1 beta (IL-1β), and malondialdehyde (MDA) in the hippocampus of septic mice and increased the activity of superoxide dismutase (SOD) and catalase (CAT) enzymes. YBTF could also upregulate the mRNA expression of SOD1, SOD2, CAT, and forkhead box O1 (FOXO1) and downregulate the mRNA expression of TNF-α, IL-1β, nuclear factor kappa-B (NF-κB), p53, and SIRT1 in the hippocampus of septic mice. The animal experiment results showed that YBTF could improve the cognitive dysfunction of septic mice. The effect of YBTF was weaker than that of dexamethasone, but it could enhance the improvement effect when used in conjunction with dexamethasone. The component analysis results showed that YBTF contained 9 compounds, including catechin, gallocatechin gallate, rutin, hyperoside, epicatechin gallate, dihydroquercetin, quercetin, myricetin, and sulphuretin. From these results, YBTF could activate SIRT1 through its active compound components to improve the cognitive dysfunction of septic mice.

Highlights

Sepsis is a systemic inflammation caused by the host’s unregulated response to infection, which will cause systemic inflammation network effects, gene polymorphisms, immune dysfunction, abnormal blood coagulation, tissue damage, and the body’s abnormal response to different infectious pathogenic microorganisms and their toxins [1]
One week after the induction of sepsis, no death was found in the normal group, but there were 8 deaths in the model group, 3 deaths in the Yunnan black tea flavonoids (YBTF) group, 4 deaths in the dexamethasone group, and 1 death in the YBTF + dexamethasone group (Figure 1)
Compared with the model group, the total distance travelled, the number of standing episodes, the number of self-grooming episodes, the time in the target quadrant, and the number of times the mice crossed the region were significantly increased (P < 0.05) in the model group, and the latency time was significantly increased (P < 0.05) in the dexamethasone, YBTF, and YBTF + dexamethasone groups. e mice in the YBTF + dexamethasone group showed the lowest degree of cognitive impairment

Summary

Introduction

Sepsis is a systemic inflammation caused by the host’s unregulated response to infection, which will cause systemic inflammation network effects, gene polymorphisms, immune dysfunction, abnormal blood coagulation, tissue damage, and the body’s abnormal response to different infectious pathogenic microorganisms and their toxins [1]. Sepsis and its complications are the main causes of death in ICU patients with a fatality rate of 30%–70% [3]. It has been indicated that sepsis survivors exhibit long-term cognitive impairment, including loss of memory, attention, and overall cognitive function. 70% of sepsis patients may suffer from central nervous system dysfunction secondary to sepsis [4]. Sepsis increases the risk of neurodegenerative diseases and dementia, reduces the patient’s quality of life, and places a large burden on the patient’s family

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Discussion

Conclusion