Caffeine is the most frequently used substance with a central nervous system stimulant effect, but its consumption is most often due to the intake of foods and drinks that contain it (coffee, tea, chocolate, food supplements with plant extracts of Guarana, Mate herba, Cola nuts). Due to its innocuity, caffeine is a safe xanthine alkaloid for human consumption in a wide range of doses, being used for its central nervous stimulating effect, lipolytic and diuresis-enhancing properties, but also as a permitted ergogenic compound in athletes. In addition to the mechanisms that explain the effects of caffeine on the targeted organ, there are many proposed mechanisms by which this substance would have antioxidant effects. As such, its consumption prevents the occurrence/progression of certain neurodegenerative diseases as well as other medical conditions associated with increased levels of reactive oxygen or nitrogen species. However, most studies that have assessed the beneficial effects of caffeine have used pure caffeine. The question, therefore, arises whether the daily intake of caffeine from food or drink has similar benefits, considering that in foods or drinks with a high caffeine content, there are other substances that could interfere with this action, either by potentiating or decreasing its antioxidant capacity. Natural sources of caffeine often combine plant polyphenols (phenol-carboxylic acids, catechins) with known antioxidant effects; however, stimulant drinks and dietary supplements often contain sugars or artificial sweeteners that can significantly reduce the effects of caffeine on oxidative stress. The objective of this review is to clarify the effects of caffeine in modulating oxidative stress and assess these benefits, considering the source and the dose administered.

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Caffeine and Its Antioxidant Properties—It Is All about Dose and Source

Inflammation is considered to be a crucial factor in the development of chronic diseases, eight of which were listed among the top ten causes of death worldwide in the World Health Organization’s World Health Statistics 2019. Moreover, traditional drugs for inflammation are often linked to undesirable side effects. As gentler alternatives to traditional anti-inflammatory drugs, plant-derived bioactive peptides have been shown to be effective interventions against various chronic diseases, including Alzheimer’s disease, cardiovascular disease and cancer. However, an adequate and systematic review of the structures and anti-inflammatory activities of plant-derived bioactive peptides has been lacking. This paper reviews the latest research on plant-derived anti-inflammatory peptides (PAPs), mainly including the specific regulatory mechanisms of PAPs; the structure–activity relationships of PAPs; and their enzymatic processing based on the structure–activity relationships. Moreover, current research problems for PAPs are discussed, such as the shallow exploration of mechanisms, enzymatic solution determination difficulty, low yield and unknown in vivo absorption and metabolism and proposed future research directions. This work aims to provide a reference for functional activity research, nutritional food development and the clinical applications of PAPs.

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Anti-Inflammatory Function of Plant-Derived Bioactive Peptides: A Review

Mitochondria are the main sites for oxidative phosphorylation and synthesis of adenosine triphosphate in cells, and are known as cellular power factories. The phrase “secondary mitochondrial diseases” essentially refers to any abnormal mitochondrial function other than primary mitochondrial diseases, i.e., the process caused by the genes encoding the electron transport chain (ETC) proteins directly or impacting the production of the machinery needed for ETC. Mitochondrial diseases can cause adenosine triphosphate (ATP) synthesis disorder, an increase in oxygen free radicals, and intracellular redox imbalance. It can also induce apoptosis and, eventually, multi-system damage, which leads to neurodegenerative disease. The catechin compounds rich in tea have attracted much attention due to their effective antioxidant activity. Catechins, especially acetylated catechins such as epicatechin gallate (ECG) and epigallocatechin gallate (EGCG), are able to protect mitochondria from reactive oxygen species. This review focuses on the role of catechins in regulating cell homeostasis, in which catechins act as a free radical scavenger and metal ion chelator, their protective mechanism on mitochondria, and the protective effect of catechins on mitochondrial deoxyribonucleic acid (DNA). This review highlights catechins and their effects on mitochondrial functional metabolic networks: regulating mitochondrial function and biogenesis, improving insulin resistance, regulating intracellular calcium homeostasis, and regulating epigenetic processes. Finally, the indirect beneficial effects of catechins on mitochondrial diseases are also illustrated by the warburg and the apoptosis effect. Some possible mechanisms are shown graphically. In addition, the bioavailability of catechins and peracetylated-catechins, free radical scavenging activity, mitochondrial activation ability of the high-molecular-weight polyphenol, and the mitochondrial activation factor were also discussed.

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A Comprehensive Review on Beneficial Effects of Catechins on Secondary Mitochondrial Diseases

Acute liver injury has multiple causes and can result in liver failure. In this study, we evaluated the hepatoprotective ability of cyanidin (Cy) and investigated its associated mechanisms. Cy administration significantly and dose-dependently ameliorated acute liver injury induced by carbon tetrachloride (CCl4). High-dose Cy showed effects comparable to those achieved by the positive control (silymarin). Severe oxidative stress and inflammatory responses in the liver tissue induced by CCl4 were significantly mitigated by Cy supplementation. The total antioxidant capacity and the activity of superoxide dismutase, catalase, and glutathione peroxidase were increased and the content of malondialdehyde, lipid peroxide, tumor necrosis factor α, interleukin-1β, and interleukin-6 were decreased. Additionally, the Nrf2 and NF-κB signaling pathways, which regulate antioxidative and inflammatory responses, were analyzed using quantitative real-time polymerase chain reaction and western blot assay. Cy treatment not only increased Nrf2 transcription and expression but also decreased NF-κB signaling. Moreover, molecular docking simulation indicated that Cy had high affinity for Keap1 and NF-κB/p65, which may promote nuclear translocation of Nrf2 and inhibit that of NF-κB. In summary, Cy treatment exerted antioxidative and anti-inflammatory effects and ameliorated liver injury by increasing Nrf2 and inhibiting the NF-κB pathway, demonstrating the potential of Cy as a therapeutic agent in liver injury.

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Cyanidin Alleviated CCl4-Induced Acute Liver Injury by Regulating the Nrf2 and NF-κB Signaling Pathways

Hyperuricemia (HUA) is a metabolic disease that threatens human health. Tea is a healthy beverage with an abundance of benefits. This study revealed the uric acid-lowering efficacy of six types of tea water extracts (TWEs) on HUA in mice. The results revealed that under the intervention of TWEs, the expression of XDH, a key enzyme that produces uric acid, was significantly downregulated in the liver. TWE treatment significantly upregulated the expression of uric acid secretion transporters ABCG2, OAT1, and OAT3, and downregulated the expression of uric acid reabsorption transporter URAT1 in the kidney. Furthermore, HUA-induced oxidative stress could be alleviated by upregulating the Nrf2/HO-1 pathway. The intervention of TWEs also significantly upregulated the expression of the intestinal ABCG2 protein. On the other hand, TWE intervention could significantly upregulate the expression of intestinal ABCG2 and alleviate HUA by modulating the gut microbiota. Taken together, tea can comprehensively regulate uric acid metabolism in HUA mice. Interestingly, we found that the degree of fermentation of tea was negatively correlated with the uric acid-lowering effect. The current study indicated that tea consumption may have a mitigating effect on the HUA population and provided a basis for further research on the efficacy of tea on the dosage and mechanism of uric acid-lowering effects in humans.

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Tea (Camellia sinensis) Ameliorates Hyperuricemia via Uric Acid Metabolic Pathways and Gut Microbiota

Diabetic nephropathy (DN) is the most important cause of middle and late-stage chronic kidney disease. Green tea polypeptides are extracted from tea pomace, and exhibit various pharmacological effects. In this study, we analyzed the reno-protective effects of green tea peptides in diabetic db/db mice, and explored the underlying mechanisms. Peptide treatment for 5 weeks significantly reduced the blood glucose levels and other indices of diabetes, and alleviated renal injury measured in terms of blood creatinine, urea nitrogen and urinary albumin/urinary creatinine levels. Mechanistically, the green tea peptides downregulated p-Smad2/3, α-SMA, ZO-1 and vimentin proteins in the kidney tissues, and elevated Smad7. Thus, green tea peptides inhibited the deposition of ECM proteins by suppressing excessive activation of the TGF-β/Smad signaling pathway and reducing fibronectin levels. On the other hand, tea peptides ameliorated renal injury by inhibiting the production of inflammatory factors (iNOS and TNF-α) by suppressing the NF-κB signaling pathway. In addition, we confirmed the inhibitory effect of green tea peptides on the TGF-β/Smad signaling pathway in TGF-β1-stimulated HK-2 cells. Therefore, tea peptides can be considered as an effective candidate for alleviating DN.

Green tea peptides ameliorate diabetic nephropathy by inhibiting the TGF-β/Smad signaling pathway in mice.

Background The health benefits of tea are as diverse including the reduction of uric acid levels. Xanthine oxidase is the most directly mediated enzyme in the production of uric acid. Objective To explore the inhibitory effects of different teas and its main bioactive components on the production of uric acid. Design Experimental study. The experiments were conducted in vitro using human immortalized normal liver cell line HL-7702 (L-02). Results The inhibition of the xanthine oxidase activities and the expression level of xanthine dehydrogenase mRNA stimulated in the hyperuric hepatocyte cell model showed that the unfermented green tea and th1e lightly fermented yellow tea, white tea, and oolong tea significantly stronger than the highly fermented black tea and dark tea. The main bioactive compound, gallic acid, showed the strongest inhibitory effect on uric acid production, followed by tea polyphenols and theaflavins. Discussion All teas exhibited significant inhibition of xanthine oxidase activities, and the degree of fermentation of tea may be inversely proportional to its ability to inhibit the production of uric acid. Compared with tea polyphenols rich in tea, gallic acid may be a more potential uric acid-lowering component. Conclusion In this article, we first compared the effects of six traditional Chinese tea made from a single variety in stabilizing the synthesis of uric acid and found that the lighter the fermentation, the greater the potential for inhibiting the production of uric acid. Furthermore, we analyzed the inhibitory effects of its main biochemical active ingredients and found that the inhibitory effects of polyphenols rich in lightly fermented tea were significantly stronger than caffeine rich in highly fermented tea. Our findings will be helpful for people to choose a proper tea for alleviating hyperuricemia and provide a scientific basis for uric acid-lowering tea processing.

https://foodandnutritionresearch.net/index.php/fnr/article/download/8239/14679

Tea and its components reduce the production of uric acid by inhibiting xanthine oxidase

Liver injury is a life-threatening condition that is usually caused by excessive alcohol consumption, improperdiet, and stressful lifestyle and can even progress to liver cancer. Tea is a popular beverage with proven health benefits and is known to exert a protective effect on the liver, intestines, and stomach. In this study, we analyzed the therapeutic effects of six kinds of tea on carbon tetrachloride (CCl4)-induced liver injury in a mouse model. The mice were injected with 10 mL/kg 5% CCl4 to induce liver injury and then given oral gavage of green tea, yellow tea, oolong tea, white tea, black tea, and dark tea, respectively. The serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured, and the expression levels of inflammation and oxidative stress-related proteins in the liver tissues were quantified. All six kinds of tea partly reduced the liver index, restored the size of the enlarged liver in the CCl4 model, and decreased the serum levels of ALT and AST. Furthermore, the highly fermented dark tea significantly reduced the expression levels of NF-κB and the downstream inflammatory factors, whereas the unfermented green tea inhibited oxidative stress by activating the antioxidant Nrf2 pathway. Taken together, tea can protect against liver inflammation, and unfermented tea can improve antioxidant levels. Further studies are needed on the bioactive components of tea to develop drugs against liver injury.

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Chinese Tea Alleviates CCl4-Induced Liver Injury through the NF-κBorNrf2Signaling Pathway in C57BL-6J Mice

Extract of Jasminum grandiflorum L. alleviates CCl4-induced liver injury by decreasing inflammation, oxidative stress and hepatic CYP2E1 expression in mice.

Lingli Sun

Papers

Green tea peptides ameliorate diabetic nephropathy by inhibiting the TGF-β/Smad signaling pathway in mice.

Tea and its components reduce the production of uric acid by inhibiting xanthine oxidase

Chinese Tea Alleviates CCl4-Induced Liver Injury through the NF-κBorNrf2Signaling Pathway in C57BL-6J Mice

Extract of Jasminum grandiflorum L. alleviates CCl4-induced liver injury by decreasing inflammation, oxidative stress and hepatic CYP2E1 expression in mice.

Tea (Camellia sinensis) Ameliorates Hyperuricemia via Uric Acid Metabolic Pathways and Gut Microbiota