Carapax Trionycis extracts inhibit fibrogenesis of activated hepatic stellate cells via TGF-β1/Smad and NFκB signaling

Hu, Zuliang; Peng, You; Xiong, Shiyun; Gao, Jianrong; Tang, Yinping; Ye, Xiaochuan; Yu, Xiang; Zhang, Dongquan

doi:10.1016/j.biopha.2017.08.011

Cited by 25 publications

(18 citation statements)

References 28 publications

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“…Carapax Trionycis contains animal gum, keratin, iodine, vitamin D, and other ingredients. Carapax Trionycis and its active ingredients can inhibit the TGF-β1-induced proliferation of HSC-T6 cells to exert anti-fibrotic effects 37 . Moreover, a new heptapeptide from Carapax trionycis is beneficial in carbon tetrachloride-induced acute liver injury in mice 38 .…”

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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“…TGF-β signal transduction involves TGF-β1 binding to type II TGF-β receptors (TβRII), followed by recruitment and activation of type I TGF-β receptors (TβRI) [29]. Activated TβRI phosphorylates smad2 and smad3, and then forms complexes with smad4, which translocates into the nucleus and binds to smad binding element (SBE) to activate HSCs [6].…”

Section: Pa Reduces Tgf-β1-induced Hscs Activation By Blocking a Smadmentioning

confidence: 99%

“…In contrast, smad7 acts as a smad inhibitor by inhibiting the TGF-β1-dependent SMAD signaling pathway by interfering with smad2 and smad3 phosphorylation via TβRI [29,30]. To examine the effects of PA on TGF-β1-reduced smad7 expression, we first determined the timing and concentration of smad7 in HSC-T6 cells.…”

Section: Pa Reduces Tgf-β1-induced Hscs Activation By Blocking a Smadmentioning

confidence: 99%

Platyconic Acid A, Platycodi Radix-Derived Saponin, Suppresses TGF-β1-Induced Activation of Hepatic Stellate Cells via Blocking SMAD and Activating the PPARγ Signaling Pathway

Choi

Kim

Lee

et al. 2019

Cells

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Platycodi radix is a widely sold health food worldwide, which contains numerous phytochemicals that are beneficial to health. Previously, we reported that saponin from the roots of Platycodi radix-derived saponin inhibited toxicant-induced liver diseases. Nevertheless, the inhibitory effect of platyconic acid A (PA), the active component of Platycodi radix-derived saponin, on the anti-fibrotic activity involving the SMAD pathway remains unclear. We investigated the inhibitory effects of PA on TGF-β1-induced activation of hepatic stellate cells (HSCs). PA inhibited TGF-β1-enhanced cell proliferation, as well as expression of α-SMA and collagen Iα1 in HSC-T6 cells. PA suppressed TGF-β1-induced smad2/3 phosphorylation and smad binding elements 4 (SBE4) luciferase activity. Reversely, PA restored TGF-β1-reduced expression of smad7 and peroxisome proliferator-activated receptor (PPAR)γ. PA also repressed TGF-β1-induced phosphorylation of Akt and MAPKs. In summary, the results suggest that the inhibitory effect of PA on HSCs occurs through the blocking of SMAD-dependent and SMAD-independent pathways, leading to the suppression of α-SMA and collagen Iα1 expression.

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“…Intriguingly, the cytotoxicity of CDK was specific to cancer cells, because CDK did not influence the viability of FHs 74 Int cells, suggesting that CBK may cause less adverse events in clinical settings. In addition, it is reported that Carapax Trionycis inhibits fibrogenesis of activated hepatic stellate cells [8], and Radix Astragali protects against podocyte injury in nephrotic syndrome [9]. The above data demonstrate that CBK is potentially superior to some chemotherapeutic anti-cancer agents, in terms of causing side effects.…”

Section: Discussionmentioning

confidence: 92%

Compound Bieshe Kang’ai inhibits proliferation and induces apoptosis in HCT116 human colorectal cancer cells

Wan¹,

Tan²,

Li³

et al. 2019

Trop. J. Pharm Res

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Purpose: To study the effect of Compound Bieshe Kang'ai (CBK) on proliferation and apoptosis in colorectal cancer cells. Methods: HCT116 colorectal cancer cells and FHs 74 Int intestinal cells were treated with CBK, followed by determination of cell proliferation with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Caspase-9 and caspase-3 activities as well as protein expressions of Bcl-2 and BAX, and mRNA levels of caspase-9, caspase-3, Bcl-2 and BAX in HCT116 cells were evaluated, followed by examination of the morphological alterations of HCT116 cells with Hoechst 33342 staining. Results: CBK suppressed proliferation of HCT116 cells in a concentration-and time-dependent pattern, without cytotoxicity to FHs 74 Int cells. CBK also elevated caspase-9 and caspase-3 activities, mitigated protein translation of Bcl-2 and augmented that of BAX. It also enhanced mRNA transcriptions of caspase-9, caspase-3 and BAX, but decreased that of Bcl-2 in HCT116 cells in a concentrationdependent manner, as well as induced cancer cell shrinkage, nuclear fragmentation and chromatin condensation. Conclusion: The findings highlight CBK as a promising therapeutic agent for colorectal cancers, by retarding proliferation and inducing apoptosis in cancer cells.

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Carapax Trionycis extracts inhibit fibrogenesis of activated hepatic stellate cells via TGF-β1/Smad and NFκB signaling

Cited by 25 publications

References 28 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

Platyconic Acid A, Platycodi Radix-Derived Saponin, Suppresses TGF-β1-Induced Activation of Hepatic Stellate Cells via Blocking SMAD and Activating the PPARγ Signaling Pathway

Compound Bieshe Kang’ai inhibits proliferation and induces apoptosis in HCT116 human colorectal cancer cells

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