Glycyrrhizic acid pretreatment prevents sepsis-induced acute kidney injury via suppressing inflammation, apoptosis and oxidative stress

Zhao, Hongyu; Liu, Zhenning; Shen, Haitao; Jin, Shuai; Zhang, Shun

doi:10.1016/j.ejphar.2016.04.006

Cited by 60 publications

(40 citation statements)

References 21 publications

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“…In tumors, GA promotes apoptosis, while during liver, brain or kidney injury, it impedes apoptosis. [26][27][28] It is well known that caspase family of proteins plays an important role in the progression of apoptosis. Caspase-dependent apoptosis is a "waterfall pattern" cascade reaction beginning with the activation of initiator-like caspase-2, −8, −9, and −10 enzymes and is continued with the increase in their expression levels.…”

Section: Discussionmentioning

confidence: 99%

<p>Glycyrrhizic Acid Inhibits Proliferation of Gastric Cancer Cells by Inducing Cell Cycle Arrest and Apoptosis</p>

Wang¹,

Ge²,

Qu³

et al. 2020

CMAR

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Glycyrrhizic acid (GA) is the main active ingredient extracted from Chinese herb licorice root, and it shows anti-tumor effects in many cancer types, while its role in gastric cancer (GC) is still unknown. In this study, we evaluated the effects of GA on GC cells and explored the underlying mechanisms. Methods: The anti-proliferation effect of GA on GC cells was assessed by CCK-8, colony formation, and EdU assay. The effects of GA on cell cycle and apoptosis were detected by flow cytometer. Western blotting was performed to explore the underlying mechanisms. Results: Our results showed that GA had a time-and dose-dependent inhibitory effect on proliferation of GC cells. Flow cytometer analysis demonstrated that GA would lead to G1/ S-phase arrest and apoptosis. GA treatment down-regulated the levels of G1 phase-related proteins, including cyclin D1, D2, D3, E1, and E2. In terms of apoptosis, GA treatment upregulated the levels of Bax, cleaved PARP, and pro-caspase-3,-8,-9, but did not influence their cleavage patterns. The expression of Bcl-2, survivin and p65 was attenuated after treatment. Besides, GA would down-regulate the phosphorylation of PI3K/AKT pathway. Conclusion: This study focused on inhibitory effect of GA on GC cells by inducing cell cycle arrest and apoptosis. Several important cyclins-and apoptosis-related proteins were involved in the regulation of GA to GC cells, and phosphorylated PI3K and AKT were attenuated. The results of this study indicated that GA is a potential and promising anticancer drug for GC.

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Section: Discussionmentioning

confidence: 99%

<p>Glycyrrhizic Acid Inhibits Proliferation of Gastric Cancer Cells by Inducing Cell Cycle Arrest and Apoptosis</p>

Wang¹,

Ge²,

Qu³

et al. 2020

CMAR

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“…The TLR4 signalling pathway is activated at the initiation of LPS‐induced inflammatory response, then its downstream pathway NF‐κB is activated, and NF‐κB activation induces the release of inflammatory factors . When the inflammatory factors in the cells are released, the inactive NF‐κB in the cytoplasm is rapidly transferred to the nucleus to regulate the inflammatory cytokines . Therefore, the TLR4 signalling pathway can be considered an effective therapeutic target for AKI induced by LPS.…”

Section: Discussionmentioning

confidence: 99%

“…[14] When the inflammatory factors in the cells are released, the inactive NF-jB in the cytoplasm is rapidly transferred to the nucleus to regulate the inflammatory cytokines. [15,16] Therefore, the TLR4 signalling pathway can be considered an effective therapeutic target for AKI induced by LPS.…”

Section: Discussionmentioning

confidence: 99%

S-nitrosoglutathione protects lipopolysaccharide-induced acute kidney injury by inhibiting toll-like receptor 4–nuclear factor-κB signal pathway

Fan

Zhao²,

Zhu

2019

Journal of Pharmacy and Pharmacology

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Objectives To investigate the therapeutic effects and mechanisms of S‐nitrosoglutathione (SNG) on acute kidney injury (AKI) induced by lipopolysaccharide (LPS). Methods We established an AKI model by intraperitoneal administration of LPS in mice and LPS‐induced human kidney (HK‐2) cells in vitro. We obtained the kidney tissues from mice for histopathological examination, examined inflammatory cytokines by enzyme‐linked immunosorbent assay and measured the expression levels of toll‐like receptor 4–nuclear factor‐κB (TLR4–NF‐κB) signal pathway‐related proteins by Western blotting. Key findings Pretreatment of SNG effectively improved the kidney function, reduced the pathological damage score of kidney in mice and decreased the expression levels of IL‐1β, IL‐6 and TNF‐α in a dose‐dependent manner in vivo and in vitro. Furthermore, pretreatment of SNG also repressed TLR4, phosphorylated NF‐κB IκBα, IKKβ and p65 expression levels in HK‐2 cells induced by LPS. Conclusions S‐nitrosoglutathione attenuates the severity of LPS‐induced AKI by inhibiting the TLR4–NF‐κB signalling pathway and may act as a protective agent for septic AKI.

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“…The HBZY-1 cell line was obtained from the Cell Bank of Chinese Academy of Sciences (Shanghai, China) and incubated with Dulbecco's modified Eagle's/F-12 medium [10% (v/v) fetal calf serum and 1% (v/v) antibiotics mixture] in 95% air and 5% CO 2 at 37°C ( 13 ). Specific pathogen-free (SPF), male Sprague-Dawley (SD) rats (weighing 280–320 g, 9 weeks old) were provided by the Laboratory Animal Center of Anhui Medical University (Hefei, China).…”

Section: Methodsmentioning

confidence: 99%

In�vitro and in�vivo study of the expression of the Syk/Ras/c‑Fos pathway in chronic glomerulonephritis

et al. 2018

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Chronic glomerulonephritis (CGN) is the most common form of glomerular disease; however, its associated molecular mechanisms remain unclear. Spleen tyrosine kinase (Syk) is a key mediator of B-receptor signaling on the surface of inflammatory cells. The primary target for R406 is Syk. The aim of the present study was to investigate the molecular mechanisms involved in a rat model of CGN induced by adriamycin (ADR) and in the rat glomerular mesangial cell line, HBZY-1, stimulated by lipopolysaccharide (LPS). CGN was induced in the rat models by two intravenous injections of ADR into the tail: 3.5 mg/kg ADR was given on the first day and 3.0 mg/kg on the fourteenth day. HBZY-1 cells were incubated with 0.5 µg/ml LPS for 48 h. The pathological alterations in the kidney tissues were observed by hematoxylin and eosin staining. The 24 h urinary protein, blood urea nitrogen (BUN) and creatinine levels were measured using an automatic biochemistry analyzer. The mRNA expression levels of Syk, Ras, mitogen activated protein kinase kinase (MEK), extracellular signal regulated kinase (ERK)1/2 and c-Fos was measured by reverse transcription-quantitative polymerase chain reaction. Subsequently, the protein levels of phosphorylated (p)-Syk, Ras, p-MEK1/2, p-ERK1/2 and c-Fos were measured by western blot analysis. In the model group, 24 h urinary protein, BUN and creatinine levels were increased when compared with the normal group (P<0.05). In addition, compared with the normal group, the mRNA and protein levels of the Syk/Ras/c-Fos pathway components in vitro and in vivo were markedly increased, inhibiting the abnormal cell viability of mesangial cells. In conclusion, the results of the present study suggested a potential role for the Syk/Ras/c-Fos signaling pathway in CGN, which indicated the necessity for further investigation at the clinical level.

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Glycyrrhizic acid pretreatment prevents sepsis-induced acute kidney injury via suppressing inflammation, apoptosis and oxidative stress

Cited by 60 publications

References 21 publications

<p>Glycyrrhizic Acid Inhibits Proliferation of Gastric Cancer Cells by Inducing Cell Cycle Arrest and Apoptosis</p>

<p>Glycyrrhizic Acid Inhibits Proliferation of Gastric Cancer Cells by Inducing Cell Cycle Arrest and Apoptosis</p>

S-nitrosoglutathione protects lipopolysaccharide-induced acute kidney injury by inhibiting toll-like receptor 4–nuclear factor-κB signal pathway

In�vitro and in�vivo study of the expression of the Syk/Ras/c‑Fos pathway in chronic glomerulonephritis

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