BuShenKangShuai Tablet Alleviates Hepatic Steatosis via Improving Liver Adiponectin Resistance in ApoE-/- Mice
| Autor: | Mei-ling Chen, Shuo Wang, Hui Wang, Junping Zhang, Hui-yun Jia, Li-yuan Bi, Shu-chao Pang, Yuan-yuan Wang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
medicine.medical_specialty
Article Subject Atorvastatin Blood lipids Proinflammatory cytokine 03 medical and health sciences 0302 clinical medicine Internal medicine Nonalcoholic fatty liver disease medicine 030304 developmental biology 0303 health sciences Adiponectin business.industry lcsh:Other systems of medicine medicine.disease lcsh:RZ201-999 Endocrinology Complementary and alternative medicine TLR4 030211 gastroenterology & hepatology Steatosis business Dyslipidemia Research Article medicine.drug |
| Zdroj: | Evidence-Based Complementary and Alternative Medicine, Vol 2019 (2019) Evidence-based Complementary and Alternative Medicine : eCAM |
| ISSN: | 1741-4288 |
| Popis: | BuShenKangShuai tablet (BSKS) is a Chinese herbal compound, which has been used to treat nonalcoholic fatty liver disease and cardiovascular diseases in clinic for over four decades. This study intends to explore whether BSKS administration can alleviates hepatic steatosis via improving liver adiponectin resistance in ApoE-/- mice. ApoE-/- mice were fed with western-type diet for 6 weeks and then were administrated with BSKS or atorvastatin for 6 weeks by gavage, and then blood and liver were collected for analysis. The results showed that BSKS attenuated hepatic steatosis, decreased blood lipids, and increased the serum level of adiponectin. We also found that adiponectin resistance in the liver was improved by BSKS, while the expression of TLR4 and NF-κB p65 was inhibited, followed by the suppression of proinflammatory mediators of TNF-α. Our data provided evidence that BSKS was able to alleviate hepatic steatosis in vivo. The underlying mechanism of BSKS was focused on improving liver adiponectin resistance, thereby regulating dyslipidemia and inhibiting inflammatory signaling pathway. |
| Databáze: | OpenAIRE |
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