Ferulic acid suppresses activation of hepatic stellate cells through ERK1/2 and Smad signaling pathways in vitro

Xu, Tianjiao; Pan, Zhi; Dong, Miaoxian; Yu, Chunlei; Niu, Yingcai

doi:10.1016/j.bcp.2014.10.016

Cited by 30 publications

(21 citation statements)

References 46 publications

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“…Approximately 1 mL of 2.5% glutaraldehyde was added slowly to fix the cell pellet for more than 2 hours. Experimental sample handling methods were described in the reference . For electron microscopy, 70‐90 nm sections were collected on copper grids and stained with 5% uranyl acetate and Renault's lead citrate .…”

Section: Methodsmentioning

confidence: 99%

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Cadmium induces actin cytoskeleton alterations and dysfunction in Neuro‐2a cells

Song

Chen

et al. 2019

Environmental Toxicology

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Cadmium (Cd) is considered a possible etiological factor in neurodegenerative diseases. However, the exact mechanism by which Cd induces neurotoxicity is not well elucidated. In this study, Neuro-2a cells were treated with 0, 10, 20, and 40 μM cadmium chloride for 24 hours to investigate the effects of Cd on the cytoskeleton of nerve cells. MTT assay and ELISA assay were used to examine cell viability and release of lactate dehydrogenase (LDH) from cells, respectively. Results showed that Cd reduced cell viability and increased the release of LDH in a dose-dependent manner (P < 0.05). The morphology of treated cell was damaged as indicated by cell collapse and dimensionality reduction. Moreover, the axonal spines and normal features of Cd-treated neurons disappeared. We checked the ultrastructure of Neuro-2a cells and found that Cd-induced swelling, membrane damage, overflow of cytoplasm contents, and cell fragmentation. Damaged mitochondria, expanded endoplasmic reticulum, and abnormal microfilaments were found in Cd-treated cells rather than in untreated cells. Compared with the control group, the relative release of glutamate in the supernatant after Cd treatment was reduced, indicating that Cd exposure could reduce the release of glutamate by inhibiting the function of nerve-2a cells. Cd decreased the mRNA and protein expression levels of cytoskeletal proteins including DBN, SYP, and TAU, which might promote cytoskeleton alterations in Cd-treated cells. In conclusion, Cd-induced actin cytoskeleton alterations and dysfunction of cultured neurons. The results of the present study provide new insights for the investigation of Cd-induced neurotoxicity.

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Section: Methodsmentioning

confidence: 99%

“…Complementary DNA synthesis was performed using primeScript RT reagent kit (Takara Biotechnology, Dalian, China). Real‐time PCR was carried out using SYBR green as previously described . The primers used in real‐time PCR were as follows (Table ).…”

Section: Methodsmentioning

confidence: 99%

Cadmium induces actin cytoskeleton alterations and dysfunction in Neuro‐2a cells

Song

Chen

et al. 2019

Environmental Toxicology

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“…Primary mouse HSCs received Lipofectamine 2000 (Life Technologies) with TGF-β1/Smad responsive reporter genes REPO TM SMAD (Genomeditech Co., shanghai, China) as previous described 13 . Transfection efficiency was normalized by cotransfection of Renilla luciferase reporter plasmid pRL-TK (Promega, Madison, WI).…”

Section: Methodsmentioning

confidence: 99%

ENMD-1068 inhibits liver fibrosis through attenuation of TGF-β1/Smad2/3 signaling in mice

Sun

Wang

Zhang

et al. 2017

Sci Rep

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Protease-activated receptor 2 (PAR-2) plays an important role in the pathogenesis of liver fibrosis. We studied the effect of N1-3-methylbutyryl-N4-6-aminohexanoyl-piperazine (ENMD-1068), a PAR-2 antagonist, on the development of CCl4-induced liver fibrosis in mice and activation of hepatic stellate cells (HSCs) isolated from the mice. Before CCl4 injection, the mice were injected intraperitoneally with either 25 mg/kg or 50 mg/kg ENMD-1068 or with 200 μL of the vehicle control twice per week for 4 weeks. The isolated HSCs were stimulated by TGF-β1 with or without ENMD-1068 to evaluate the role of PAR-2 in TGF-β1 induced HSCs activation and collagen production. We showed that the levels of ALT/AST, collagen content, and α-smooth muscle actin (α-SMA) were significantly reduced by treatment with ENMD-1068 in CCl4-induced fibrotic mice. Interestingly, we found TGF-β1 signaling-related expression levels of α-SMA, type I and III collagen, and C-terminal phosphorylation of Smad2/3 were significantly decreased in the ENMD-1068 treated HSCs. Moreover, we showed ENMD-1068 treatment inhibited trypsin or SLIGRL-NH2 stimulated calcium release and TGF-β1 induced Smad transcriptional activity in HSCs. We demonstrated that ENMD-1068 reduces HSCs activation and collagen expression through the inhibiton of TGF-β1/Smad signal transduction.

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“…Gao et al investigate the antifibrotic effects of DBT on bleomycin-induced pulmonary fibrosis in rats and found that DBT administration attenuated the degree of alveolitis and lung fibrosis and markedly reduced the mRNA levels of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) [27]. Xu et al demonstrated that administration of FA significantly decreased the levels of collagen and tissue inhibitor of metalloproteinases (TIMPs) and positively modulated the expression of matrix metalloproteinases (MMPs) in liver fibrosis induced by alcoholic and polyunsaturated fatty acid [52]. These results proved that the mechanisms of multitargets of traditional Chinese medicine can be better used for antifibrotic treatment.…”

Section: Discussionmentioning

confidence: 99%

Danggui Buxue Tang Attenuates Tubulointerstitial Fibrosis via Suppressing NLRP3 Inflammasome in a Rat Model of Unilateral Ureteral Obstruction

Wang

Guo³

et al. 2016

BioMed Research International

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Inflammation significantly contributes to the progression of chronic kidney disease (CKD). This study aimed to characterize Danggui Buxue Tang (DBT) renoprotection and relationship with NOD-like receptors family pyrin domain-containing 3 (NLRP3) inflammasome expression in rats with unilateral ureteral obstruction (UUO). Sprague-Dawley rats were subjected to UUO and randomly assigned to untreated UUO, enalapril-treated (10 mg/kg/day), and DBT-treated (9 g/kg/day) groups. Sham-operated rats served as controls, with 8 rats in each group. All rats were sacrificed for blood and renal specimen collection at 14 days after UUO. Untreated UUO rats exhibited azotemia, intense tubulointerstitial collagen deposition, upregulations of tubulointerstitial injury index, augmentation levels of collagen I (Col I), α-smooth muscle actin (α-SMA), NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), pro-caspase-1, caspase-1, IL-1β, and pro-IL-1β. DBT treatment significantly attenuated interstitial collagen deposition and tubulointerstitial injury, lowering Col I and α-SMA levels. Synchronous expressions of NLRP3, ASC, pro-caspase-1, caspase-1, pro-IL-1β, and IL-1β decreased in renal tissue. In comparison to enalapril, DBT significantly reduced tubulointerstitial injury, interstitial collagen deposition, and expressions of Col I and IL-1β. Thus, DBT offers renoprotection in UUO rats, which was associated with suppressing NLRP3 inflammasome expression and following reduction of the secretion of cytokine IL-1β. The mechanisms of multitargets of traditional Chinese medicine can be better used for antifibrotic treatment.

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Ferulic acid suppresses activation of hepatic stellate cells through ERK1/2 and Smad signaling pathways in vitro

Cited by 30 publications

References 46 publications

Cadmium induces actin cytoskeleton alterations and dysfunction in Neuro‐2a cells

Cadmium induces actin cytoskeleton alterations and dysfunction in Neuro‐2a cells

ENMD-1068 inhibits liver fibrosis through attenuation of TGF-β1/Smad2/3 signaling in mice

Danggui Buxue Tang Attenuates Tubulointerstitial Fibrosis via Suppressing NLRP3 Inflammasome in a Rat Model of Unilateral Ureteral Obstruction

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