scholarly journals Supplementation with lower doses of EGCg reduces liver injury markers of type 2 diabetic rats

2019 ◽  
Vol 6 (1) ◽  
pp. 15-23
Author(s):  
Kazuki Mochizuki ◽  
Yu Tan ◽  
Yumiko Uchiyama ◽  
Takuji Suzuki ◽  
Natsuyo Hariya ◽  
...  
2019 ◽  
Vol 72 (1-2) ◽  
pp. 1900203
Author(s):  
Liyan Zhao ◽  
Qifang Zheng ◽  
Yalu Zou ◽  
Yuanyuan Wang ◽  
Yuntang Wu ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Biyu Hou ◽  
Yuerong Zhao ◽  
Guifen Qiang ◽  
Xiuying Yang ◽  
Chunyang Xu ◽  
...  

Lipid metabolism disorder and inflammation are essential promoters in pathogenesis of liver injury in type 2 diabetes. Puerarin (PUR) has been reported to exert beneficial effects on many diabetic cardiovascular diseases and chemical-induced liver injuries, but its effects on diabetic liver injury and its mechanism are still unclear. The current study was designed to explore the therapeutic effect and mechanism of PUR on liver injury in a type 2 diabetic rat model induced by a high-fat diet combined with low-dose streptozotocin. The diabetic rats were treated with or without PUR (100 mg/kg/day) by gavaging for 8 weeks, and biochemical and histological changes in liver were examined. Results showed that treatment with PUR significantly attenuated hepatic steatosis by regulating blood glucose and ameliorating lipid metabolism disorder. Liver fibrosis was relieved by PUR treatment. PUR inhibited oxidative stress and inflammation which was associated with inactivation of NF-κB signaling, thereby blocking the upregulation of proinflammatory cytokines (IL-1β, TNF-α) and chemokine (MCP-1). This protection of PUR on diabetic liver injury is possibly related with inhibition on TGF-β/Smad signaling. In conclusion, the present study provides evidence that PUR attenuated type 2 diabetic liver injury by inhibiting NF-κB-driven liver inflammation and the TGF-β/Smad signaling pathway.


2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Li-ping Han ◽  
Chun-jun Li ◽  
Bei Sun ◽  
Yun Xie ◽  
Yue Guan ◽  
...  

Immune and inflammatory pathways play a central role in the pathogenesis of diabetic liver injury. Celastrol is a potent immunosuppressive and anti-inflammatory agent. So far, there is no evidence regarding the mechanism of innate immune alterations of celastrol on diabetic liver injury in type 2 diabetic animal models. The present study was aimed at investigating protective effects of celastrol on the liver injury in diabetic rats and at elucidating the possible involved mechanisms. We analyzed the liver histopathological and biochemical changes and the expressions of TLR4 mediated signaling pathway. Compared to the normal control group, diabetic rats were found to have obvious steatohepatitis and proinflammatory cytokine activities were significantly upregulated. Celastrol-treated diabetic rats show reduced hepatic inflammation and macrophages infiltration. The expressions of TLR4, MyD88, NF-κB, and downstream inflammatory factors IL-1βand TNFαin the hepatic tissue of treated rats were downregulated in a dose-dependent manner. We firstly found that celastrol treatment could delay the progression of diabetic liver disease in type 2 diabetic rats via inhibition of TLR4/MyD88/NF-κB signaling cascade pathways and its downstream inflammatory effectors.


2021 ◽  
Vol 85 ◽  
pp. 104657
Author(s):  
Fuqiang Zhao ◽  
Kexue Zhu ◽  
Qiancheng Zhao ◽  
Qibing Liu ◽  
Jun Cao ◽  
...  

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 643-P ◽  
Author(s):  
YANFEI HAN ◽  
LINDONG LI ◽  
YANJUN LIU ◽  
YOU WANG ◽  
CHUNHUA YAN ◽  
...  

2010 ◽  
Vol 8 (4) ◽  
pp. 293-297 ◽  
Author(s):  
Teng GUAN ◽  
Yi-Song QIAN ◽  
Meng-Hao HUANG ◽  
Long-Fei HUANG ◽  
Xu-Zhen TANG ◽  
...  

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