Uncovering the antioxidant characteristics of black tea by coupling in vitro free radical scavenging assay with UHPLC–HRMS analysis

Chen, Ning; Han, Binsong; Fan, Xiaowei; Cai, Fang; Ren, Fandong; Xu, Meilin; Zhong, Jing; Zhang, Yi; Ren, Dabing; Yi, Lunzhao

doi:10.1016/j.jchromb.2020.122092

Cited by 23 publications

(10 citation statements)

References 39 publications

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“…A number of studies have revealed the treatment efficacy of TF in various diseases, such as cardiovascular disease 8 , inflammatory disorders 9 , fatty liver 10 , and bacterial and viral infection 11 . These beneficial effects have been attributed to the regulation of endogenic antioxidant systems and scavenging of excessive ROS 12 , 13 . Recently, TF has been reported to improve the activities of key enzymes of carbohydrate metabolism in diabetic rats, exhibiting renal protective effects via its antioxidant activity 14 .…”

Section: Introductionmentioning

confidence: 99%

Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1

Ye¹,

Yang²,

Liu³

et al. 2021

Int. J. Biol. Sci.

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Renal tubular cell injury induced by calcium oxalate (CaOx) is a critical initial stage of kidney stone formation. Theaflavin (TF) has been known for its strong antioxidative capacity; however, the effect and molecular mechanism of TF against oxidative stress and injury caused by CaOx crystal exposure in kidneys remains unknown. To explore the potential function of TF on renal crystal deposition and its underlying mechanisms, experiments were conducted using a CaOx nephrocalcinosis mouse model established by glyoxylate intraperitoneal injection, and HK-2 cells were subjected to calcium oxalate monohydrate (COM) crystals, with or without the treatment of TF. We discovered that TF treatment remarkably protected against CaOx-induced kidney oxidative stress injury and reduced crystal deposition. Additionally, miR-128-3p expression was decreased and negatively correlated with SIRT1 level in mouse CaOx nephrocalcinosis model following TF treatment. Moreover, TF suppressed miR-128-3p expression and further abolished its inhibition on SIRT1 to attenuate oxidative stress in vitro. Mechanistically, TF interacted with miR-128-3p and suppressed its expression. In addition, miR-128-3p inhibited SIRT1 expression by directly binding its 3'-untranslated region (UTR). Furthermore, miR-128-3p activation partially reversed the acceerative effect of TF on SIRT1 expression. Taken together, TF exhibits a strong nephroprotective ability to suppress CaOx-induced kidney damage through the recovery of the antioxidant defense system regulated by miR-128-3p/SIRT1 axis. These findings provide novel insights for the prevention and treatment of renal calculus.

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Section: Introductionmentioning

confidence: 99%

Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1

Ye¹,

Yang²,

Liu³

et al. 2021

Int. J. Biol. Sci.

View full text Add to dashboard Cite

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“…Furthermore, the O − scavenging analysis was performed based on a previous method ( Chen et al, 2020 ). In brief, 3 ml Tris-HCl buffer solution (pH 8.2) was incubated in a test tube, followed by the addition of 1 ml of UB at different concentrations (20 μg/ml to 220 μg/ml), and then these mixtures were mixed with 0.3 ml of pyrogallol solution (8 mm) reagent under conditions of rapid agitation and allowed to completely react for 10 min.…”

Section: Methodsmentioning

confidence: 99%

The Gut Microbiota Metabolite Urolithin B Improves Cognitive Deficits by Inhibiting Cyt C-Mediated Apoptosis and Promoting the Survival of Neurons Through the PI3K Pathway in Aging Mice

Chen

Lei

et al. 2021

Front. Pharmacol.

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Background: Despite considerable advances in pharmacotherapy, more effective therapeutic interventions for aging-related neurodegenerative disorders (NDs), such as Alzheimer’s disease (AD), remain limited. Urolithin B (UB), one of the major subcategories of urolithins (microbiota metabolites) found in various tissues after ellagitannin consumption, has been shown to possess antioxidant, anti-inflammatory, and antiapoptotic effects. However, the neuroprotective effect of UB on brain aging in mice and its potential mechanisms were still unknown.Methods: In the current research, we first assessed the ameliorative effects of UB on oxidative injury and apoptosis induced by H2O2 in neuro-2a cells. Then a subcutaneous injection of D-galactose in mice for 8 weeks was used to establish the aging model to evaluate the protective effects of UB. The capacity of memory and learning, alterations of hippocampus histology and corresponding molecular mechanisms were all evaluated.Results: The D-gal-induced accelerated aging model in vivo demonstrated that UB could significantly ameliorate deficits in learning and memory by inhibiting the accumulation of advanced glycation end products (AGEs) and elevating the expression and activity of Cu, Zn-SOD and CAT. Furthermore, UB downregulated the c-Jun N-terminal kinase (JNK) signaling pathway and prevented cytochrome c release from isolated mitochondria, thereby inhibiting neuronal apoptosis during the aging process. More importantly, UB stimulation of aging mice activated ERK and phosphoinositide 3-kinase (PI3K), leading to neuronal survival along with Akt and p44/42 mitogen-activated protein kinase (MAPK) phosphorylation and activation.Conclusion: In summary, UB effectively alleviated cognitive deficits and ameliorated brain aging-related conditions and could be considered a healthcare product to prevent aging-associated NDs such as AD.

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“…Furthermore, the Oscavenging analysis was performed based on a previous method [20]. In brief, 3 mL Tris-HCl buffer solution (pH 8.2) was incubated in a test tube, followed by the addition of 1 mL of UB at different concentrations (20 μg/mL to 220 μg/mL), and then these mixtures were mixed with 0.3 mL of pyrogallol solution (8 mm) reagent under conditions of rapid agitation and allowed to completely react for 10 min.…”

Section: O-scavenging Testmentioning

confidence: 99%

The Gut Microbiota Metabolite Urolithin B Improves Cognitive Deficits by Inhibiting Cyt C-mediated Apoptosis and Promoting the Survival of Neurons Through the PI3K Pathway in Aging Mice

peng

Chen

Lei

et al. 2021

Preprint

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BackgroundDespite considerable advances in pharmacotherapy, more effective therapeutic interventions for aging-related neurodegenerative disorders (NDs), such as Alzheimer's disease (AD), remain limited. Urolithin B (UB), one of the major subcategories of urolithins (microbiota metabolites) found in various tissues after ellagitannin consumption, has been shown to possess antioxidant, anti-inflammatory, and antiapoptotic effects. However, the neuroprotective effect of UB on brain aging in mice and its potential mechanisms were still unknown. MethodsIn the current research, we first assessed the ameliorative effects of UB on oxidative injury and apoptosis induced by H2O2 in neuro-2a cells. Then a subcutaneous injection of D-galactose in mice for 8 weeks was used to establish the aging model to evaluate the protective effects of UB. The capacity of memory and learning, alterations of hippocampus histology and corresponding molecular mechanisms were all evaluated. ResultsThe D-gal-induced accelerated aging model in vivo demonstrated that UB could significantly ameliorate deficits in learning and memory by inhibiting the accumulation of advanced glycation end products (AGEs) and elevating the expression and activity of Cu, Zn-SOD and CAT. Furthermore, UB downregulated the c-Jun N-terminal kinase (JNK) signaling pathway and prevented cytochrome c release from isolated mitochondria, thereby inhibiting neuronal apoptosis during the aging process. More importantly, UB stimulation of aging mice activated ERK and phosphoinositide 3-kinase (PI3K), leading to neuronal survival along with Akt and p44/42 mitogen-activated protein kinase (MAPK) phosphorylation and activation. ConclusionIn summary, UB effectively alleviated cognitive deficits and ameliorated brain aging-related conditions and could be considered a healthcare product to prevent aging-associated NDs such as AD.

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Uncovering the antioxidant characteristics of black tea by coupling in vitro free radical scavenging assay with UHPLC–HRMS analysis

Cited by 23 publications

References 39 publications

Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1

Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1

The Gut Microbiota Metabolite Urolithin B Improves Cognitive Deficits by Inhibiting Cyt C-Mediated Apoptosis and Promoting the Survival of Neurons Through the PI3K Pathway in Aging Mice

The Gut Microbiota Metabolite Urolithin B Improves Cognitive Deficits by Inhibiting Cyt C-mediated Apoptosis and Promoting the Survival of Neurons Through the PI3K Pathway in Aging Mice

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