The potential roles of nitric oxide in carbon tetrachloride induced liver injury of mice and the protective effects of green tea polyphenols

Green tea polyphenols (GTPs) have been shown to exhibit diverse beneficial effects against a variety of diseases. Acetaminophen (APAP) overdose is one of the most frequent causes of drug-induced liver injury. In the current study, we aimed to investigate the protective effect of GTP on APAP-induced liver injury in mice and the underlying mechanisms involved. Male C57BL/6J mice were treated orally with different doses of GTP (37.5, 75, or 150 mg/kg) 4 h after APAP overdose (400 mg/kg) and continuously given every 8 h until sacrificed at 4, 12, 20, and 48 h after the first treatment of GTP. Survival rate and histological and biochemical assessments were performed to evaluate the APAP-induced liver injury. Protein expression of multiple drug metabolizing enzymes and transporters was measured to demonstrate the possible mechanisms involved. Our results revealed that administration of different doses of GTP significantly alleviated APAP-induced liver injury by improving the survival rate, hepatocellular necrosis, and ALT/AST/GSH levels after APAP overdose (400 mg/kg). The protein expression of APAP-induced drug transporters and metabolizing enzymes was mostly induced by GTP treatment, which was followed by reduction in drug transporters at the later time points. The current study collectively demonstrated that GTP protects against APAP-induced liver injury, possibly through regulating drug metabolizing enzymes and transporters after APAP overdose.

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Green Tea Polyphenols Decrease Enzyme Activity of Nitric Oxide Synthase

The FASEB Journal ◽

10.1096/fasebj.27.1_supplement.790.14 ◽

2013 ◽

Vol 27 (S1) ◽

Author(s):

Zhiqiang Molly Wang ◽

Conner L Tidrick ◽

Mahfuzul Haque ◽

Dennis J. Stuehr

Keyword(s):

Nitric Oxide ◽

Enzyme Activity ◽

Nitric Oxide Synthase ◽

Green Tea ◽

Tea Polyphenols ◽

Green Tea Polyphenols ◽

Oxide Synthase

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Green tea polyphenols protect PC12 cells against H2O2-induced damages by upregulating lncRNA MALAT1

International Journal of Immunopathology and Pharmacology ◽

10.1177/2058738419872624 ◽

2019 ◽

Vol 33 ◽

pp. 205873841987262 ◽

Cited By ~ 3

Author(s):

Shuheng Liu ◽

Guisheng Yu ◽

Guohua Song ◽

Qingguo Zhang

Keyword(s):

Pc12 Cells ◽

Green Tea ◽

Caspase 3 ◽

Tea Polyphenols ◽

Green Tea Polyphenols ◽

Cell Counting ◽

Signal Pathways ◽

Protective Effects ◽

Oxidative Damages ◽

Cord Injury

It is of significance to alleviate oxidative damages for the treatment of spinal cord injury (SCI). Studies have ascertained that green tea polyphenols (GTPs) exert protective activities against oxidative damages. In this study, we aimed to investigate the protective effects of GTP against H2O2-caused injuries in PC12 cells as well as the molecular underpinnings associated with long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). PC12 cells were preincubated with GTP prior to H2O2 stimulation. Furthermore, MALAT1-deficient PC12 cells were constructed by transfection and identified by quantitative real-time polymerase chain reaction (qRT-PCR) assay. Next, viability and apoptosis were detected by cell counting kit-8 and flow cytometry, respectively. Meanwhile, Western blot assay was carried out to monitor the expression alteration of proteins associated with apoptosis (Bcl-2, Bax, pro-Caspase-3/9, and cleaved Caspase-3/9) and autophagy (microtubule-associated protein 1 light chain 3 (LC3)-II, LC3-I, Beclin-1, and p62). Moreover, we examined the expression of β-catenin and dissected the phosphorylation of phosphatidylinositol 3′-kinase (PI3K) and protein kinase B (AKT). We found that H2O2 decreased the viability of PC12 cells while initiated apoptosis and autophagy processes. GTP-preincubated PC12 cells maintained the viability and resisted the apoptosis and autophagy induced by H2O2. Pointedly, GTP-pretreated PC12 cells showed an increase in MALAT1 after H2O2 stimulation. Of note, the protective effects of GTP were buffered in MALAT1-deficient cells in response to H2O2. The expression of β-catenin and phosphorylation of PI3K and AKT were upregulated by GTP, while MALAT1 knockdown led to opposite results. To sum up, GTP protected PC12 cells from H2O2-induced damages by the upregulation of MALAT1. This process might be through activating Wnt/β-catenin and PI3K/AKT signal pathways.

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