Sodium tanshinone IIA sulfonate ameliorates hepatic steatosis by inhibiting lipogenesis and inflammation

Li, Xiao Xiao; Lü, Xin; Zhang, Shi Jie; Chiu, Amy P.; Lo, Lilian H.; Largaespada, David A.; Chen, Qu Bo; Keng, Vincent W.

doi:10.1016/j.biopha.2018.12.019

Cited by 29 publications

(19 citation statements)

References 39 publications

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“…Hedyotis diffusa and its extracts have multiple anti-tumor effects in human cancers, including leukemia, liver cancer, glioblastoma, lung cancer, colon cancer, breast cancer, bladder cancer, and prostate cancer 34 ; furthermore, anti-inflammatory, antibacterial, antioxidant, anti-aging, and neuroprotective effects of Hedyotis diffusa have been reported. Emerging evidence has demonstrated that Radix salviae miltiorrhizae and its active ingredients have anti-inflammatory, antimyocardial ischemia, anti-arrhythmia, anti-platelet aggregation, anti-atherosclerosis, and anti-tumor effects; importantly, Salviae miltiorrhizae has anti-liver damage, anti-hepatic steatosis, anti-fibrosis, anti-cirrhosis and anti-HCC effects 35 , 36 . Carapax Trionycis contains animal gum, keratin, iodine, vitamin D, and other ingredients.…”

Section: Discussionmentioning

confidence: 99%

Erzhu Jiedu decoction ameliorates liver precancerous lesions in a rat model of liver cancer

Cheng¹,

Chen²,

Chen³

2020

J. Cancer

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Precancerous lesions are the intermediate stage in the development of liver cancer from cirrhosis. Early intervention measures can effectively prevent the occurrence of liver cancer and prolong the lives of patients, resulting in greater economic effects. Erzhu Jiedu decoction (EJD) is a semiempirical formula that is used in the treatment of cirrhosis and liver cancer according to the academic philosophy of “Preventive treatment of disease” and has achieved good curative effects in clinical practice. The purpose of this study was to investigate the effect of EJD on liver precancerous lesions induced by diethylnitrosamine (DEN) in rats. The results showed that EJD improved the general conditions (body weight, ALT, AST, and GGT) and reduced the number of precancerous lesions in the rat model. Notably, the medium dose of EJD (1.05 g/kg) had better treatment effects than the low dose of EJD, and the high dose of EJD did not further improve the liver lesions compared to the medium dose of EJD. Moreover, EJD effectively reduced the DEN-induced GST-Pi, AFP, CK19, c-Myc, and Ki67 protein expression in liver precancerous tissues. Interestingly, EJD significantly reduced YAP and TAZ mRNA expression in the liver precancerous lesions. Collectively, EJD protects against in the initiation of liver cancer and the regulation of c-Myc and Hippo signaling pathways may be the underlying mechanism.

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Section: Discussionmentioning

confidence: 99%

Erzhu Jiedu decoction ameliorates liver precancerous lesions in a rat model of liver cancer

Cheng¹,

Chen²,

Chen³

2020

J. Cancer

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“…Research has demonstrated that tanshinone IIA reduced fatty liver accumulation through suppression of lipogenesis and inflammation by activation of the sirtuin 1/protein kinase adenosine monophospate-activated catalytic subunit alpha 1 pathway. 45 In this current research, the HFD rat model was used to investigate the effect of tanshinone IIA on NAFLD.…”

Section: Discussionmentioning

confidence: 99%

“…34 However, its role as a potential treatment for NAFLD has not been extensively studied. 44,45 Figure 5. Oxidative status in the plasma and liver was determined by measuring superoxide dismutase (SOD), glutathione peroxidase (GSH), malondialdehyde (MDA) and catalase (CAT) protein levels using enzyme-linked immunosorbent assay kits in the three study groups: CON (normal feed for 4 months); highfat diet group (HFD for 4 months); and 2 months of HFD followed by 2 months treatment with 10 mg/kg sodium tanshinone IIA sulfonate once daily plus HFD (TAN) group (n ¼ 10 rats per group).…”

Section: Discussionmentioning

confidence: 99%

Tanshinone IIA ameliorates non-alcoholic fatty liver disease through targeting peroxisome proliferator-activated receptor gamma and toll-like receptor 4

et al. 2019

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Objective: To investigate the cellular mechanisms of action of tanshinone IIA on the fatty liver disease induced by a high-fat diet in an animal model of non-alcoholic fatty liver disease (NAFLD). Methods: Adult male Sprague Dawley rats were randomized into one of three groups: regular rat diet (CON group) for 4 months; high-fat diet (HFD group) for 4 months; HFD for 2 months followed by tanshinone IIA treatment plus HFD (TAN group) for a further 2 months. A range of physical and biochemical markers of lipid accumulation and fatty liver disease were measured and compared between the groups. Results: Tanshinone IIA treatment significantly reduced fat accumulation in the liver and plasma lipid levels that had been increased by HFD. The toll-like receptor (TLR4)/nuclear factor kappa B (NF-jB) signalling pathway was silenced by tanshinone IIA treatment. Tumour necrosis factor-a and interleukin-6 were reduced by tanshinone IIA. Hepatocyte apoptosis was inhibited by

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“…Additionally, sodium tan IIA sulfonate (STS) has a potential therapeutic role in the treatment of NAFLD, markedly suppressing lipogenesis and reducing inflammation by inhibiting the expression of sterol regulatory element binding transcription factor 1(SREBF1), fatty acid synthase (FASN), and stearoyl‐CoA desaturase (SCD) and decreasing transcriptional levels of tumor necrosis factor‐α (TNF‐α), transforming growth factor β1 (TGFβ1), and interleukin‐1β (IL‐1β) in vitro. In addition, STS decreases lipid accumulation through the activation of sirtuin 1 (SIRT1)/protein kinase AMP‐activated catalytic subunit alpha 1 (PRKAA1) pathways in vivo . Thus, tan IIA may have potential benefits in the control of fatty liver.…”

Section: Discussionmentioning

confidence: 99%

Tanshinone IIA reduces palmitate‐induced apoptosis via inhibition of endoplasmic reticulum stress in HepG2 liver cells

Wang

Hu²,

Chen

et al. 2019

Fundamemntal Clinical Pharma

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Research has indicated that stress on the endoplasmic reticulum (ER) of a cell affects the pathogenesis of metabolic disorders such as obesity, type 2 diabetes mellitus, and non‐alcoholic fatty liver disease (NAFLD). Palmitate, a saturated fatty acid, is known to induce toxicity and cell death in various types of cells. Tanshinone IIA (Tan IIA), one of the effective components of the traditional Chinese medicine Danshen, was reported to exhibit a variety of biochemical activities, including amelioration of ER stress‐mediated apoptosis in renal preservation. To address the hypothesis that tan IIA attenuates apoptosis and triglycerides (TG) accumulation via reducing ER stress, we studied the effect of tan IIA on experimentally induced ER stress using palmitate in HepG2 cells. Palmitate led to cytotoxicity, TG accumulation, and apoptosis in HepG2 cells and also strongly induced ER stress indicated by increased GRP78, phosphorylation of eIF2α, ATF6, and CHOP. Pretreatment with tan IIA (10 μm) significantly increased cell viability, decreased apoptotic cell death, and reduced the activity of caspase‐3. Meanwhile, tan IIA significantly decreased palmitate‐induced TG accumulation. Moreover, tan IIA significantly suppressed the phosphorylation of eIF2α, and inhibited GRP78, ATF6, and CHOP expression. In conclusion, tan IIA protects the HepG2 cells exposed to palmitate partially by inhibiting excessive ER stress, ER stress‐induced apoptosis, and hepatic steatosis. Therefore, tan IIA has therapeutic potential in the treatment of NAFLD.

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Sodium tanshinone IIA sulfonate ameliorates hepatic steatosis by inhibiting lipogenesis and inflammation

Cited by 29 publications

References 39 publications

Erzhu Jiedu decoction ameliorates liver precancerous lesions in a rat model of liver cancer

Erzhu Jiedu decoction ameliorates liver precancerous lesions in a rat model of liver cancer

Tanshinone IIA ameliorates non-alcoholic fatty liver disease through targeting peroxisome proliferator-activated receptor gamma and toll-like receptor 4

Tanshinone IIA reduces palmitate‐induced apoptosis via inhibition of endoplasmic reticulum stress in HepG2 liver cells

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