scholarly journals Z-Guggulsterone Induces Apoptosis in Gastric Cancer Cells through the Intrinsic Mitochondria-Dependent Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Ruxi Lv ◽  
Min Zhu ◽  
Kun Chen ◽  
Haitao Xie ◽  
Hongxia Bai ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Bax Protein ◽  
Tnf Α ◽  
Dependent Pathway ◽  
Tgf Β1 ◽  
Active Caspase

Background. To study the effects of z-guggulsterone on gastric cancer cell apoptosis and the mechanism related. Materials and Methods. Human gastric tumor SGC-7901 cells and GES-1 normal epithelial cells were treated with z-guggulsterone (0–75 μM) for 24 h. MTT assay was applied to evaluate cell proliferation. Flow cytometry and Hoechst staining were used to assess cell apoptosis. Western blotting was applied to evaluate FXR, small heterodimer partner (SHP), Bcl-2, and Bax protein expression. ELISA was applied to gain the levels of active caspase-3 and the contents of TNF-α, TGF-β1, and VEGF. Results. The expression levels of FXR and SHP were higher in tumor cells than in normal epithelial cells. Inhibition of FXR signaling with z-guggulsterone dose-dependently inhibited SGC-7901 cell proliferation and promoted SGC-7901 cell apoptosis. Bcl-2 protein expression was significantly decreased, and active caspase-3 and Bax protein expression was increased in SGC-7901 cells incubated with z-guggulsterone. The content of TNF-α was significantly increased, and the contents of VEGF and TGF-β1 were decreased in SGC-7901 cells incubated with z-guggulsterone. Conclusions. Inhibition of FXR signaling with z-guggulsterone induced anticancer effects in SGC-7901 cells by decreasing cell proliferation and promoting apoptosis. Z-guggulsterone induced cell apoptosis through the mitochondria-dependent pathway.

Isoliquiritigenin Suppresses Osteosarcoma U2OS Cell Proliferation and Invasion by Regulating the PI3K/Akt Signalling Pathway

Chemotherapy ◽  
2018 ◽  
Vol 63 (3) ◽  
pp. 155-161 ◽  
Author(s):  
Jing Chen ◽  
Cheng Liu ◽  
Qin-Qing Yang ◽  
Rui-Bin Ma ◽  
Ying Ke ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Caspase 3 ◽  
Signalling Pathway ◽  
U2os Cell ◽  
Expression Levels ◽  
Migration Assay ◽  
Invasion And Migration ◽  
U2os Cells ◽  
Active Caspase

Aims: Isoliquiritigenin (ISL) is a flavonoid, that has been shown to have antioxidant, vasorelaxant, anti-inflammatory, and antitumor activities. This study aimed to explore the antitumor effect of ISL on human osteosarcoma U2OS cells and investigate the mechanism of this effect. Methods: The effect of ISL on osteosarcoma U2OS cell proliferation, invasion, migration, and apoptosis were determined by a CCK8 assay, a transwell invasion assay, a transwell migration assay, and fluorescence-activated cell sorting, respectively. In addition, the protein expression levels of Bcl2, Bax, active Caspase-3, Akt, mTOR, p70, and Cyclin D1 were detected by western blotting. Results: ISL suppressed cell proliferation, inhibited invasion and migration, and promoted apoptosis in U2OS cells. After treatment with ISL, the protein expression levels of Bax and active Caspase-3 increased, while the level of Bcl-2 declined significantly. Furthermore, the phosphorylation levels of Akt and mTOR declined significantly compared with that of the control. Conclusion: ISL could retard proliferation and promote apoptosis of U2OS cells possibly by suppressing the PI3K/Akt signalling pathway, indicating that it might be a potential therapeutic agent for osteosarcoma treatment.

scholarly journals Resistin is a survival factor for porcine ovarian follicular cells

Reproduction ◽  
2015 ◽  
Vol 150 (4) ◽  
pp. 343-355 ◽  
Author(s):  
Agnieszka Rak ◽  
Eliza Drwal ◽  
Anna Wróbel ◽  
Ewa Łucja Gregoraszczuk
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Western Blot ◽  
Dna Fragmentation ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Inhibitory Effect ◽  
Ovarian Cell ◽  
Proliferation And Apoptosis ◽  
Mrna And Protein Expression

Previously, we demonstrated the expression of resistin in the porcine ovary, the regulation of its expression and its direct effect on ovarian steroidogenesis. The objective of this study was to examine the effect of resistin on cell proliferation and apoptosis in a co-culture model of porcine granulosa and theca cells. First, we analysed the effect of resistin at 1 and 10 ng/ml alone or in combination with FSH- and IGF1 on ovarian cell proliferation with an alamarBlue assay and protein expression of cyclins A and B using western blot. Next, the mRNA and protein expression of selected pro-apoptotic and pro-survival regulators of cell apoptosis, caspase-9, -8 and -3 activity and DNA fragmentation using real time PCR, western blot, fluorescent assay and an ELISA kit, respectively, were analysed after resistin treatment. Furthermore, we determined the effect of resistin on the protein expression of ERK1/2, Stat and Akt kinase. Using specific inhibitors of these kinases, we also checked caspase-3 activity and protein expression. We found that resistin, at both doses, has no effect on cell proliferation. The results showed that resistin decreased pro-apoptotic genes, which was confirmed on protein expression of selected factors. We demonstrate an inhibitory effect of resistin on caspase activity and DNA fragmentation. Finally, resistin stimulated phosphorylation of the ERK1/2, Stat and Akt and kinases inhibitors reversed resistin action on caspase-3 activity and protein expression to control. All of these results showed that resistin has an inhibitory effect on porcine ovarian cell apoptosis by activation of the MAPK/ERK, JAK/Stat and Akt/PI3 kinase signalling pathways.

scholarly journals miR-339-3p regulated acute pancreatitis induced by caerulein through targeting TNF receptor-associated factor 3 in AR42J cells

2020 ◽  
Vol 15 (1) ◽  
pp. 912-922
Author(s):  
Qi Wang ◽  
Shaofeng Liu ◽  
Zhen Han
Keyword(s):  
Acute Pancreatitis ◽  
Protein Expression ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Luciferase Reporter ◽  
Regulation Mechanism ◽  
Tnf Receptor ◽  
Associated Factor ◽  
Tnf Α ◽  
P38 Pathway

AbstractAcute pancreatitis (AP) is an inflammatory disease with high morbidity and mortality. The regulation mechanism of miRNA is involved in the production and development of various diseases, but the regulation mechanism of miRNA in AP is still not fully elucidated. The expression of miR-339-3p was detected using quantitative real-time PCR. The levels of TNF-α, IL-1β, and IL-6 were detected using enzyme-linked immunosorbent assay. Cell apoptosis was measured using flow cytometry. The protein expressions of TNF receptor-associated factor 3 (TRAF3), Bcl-2, C-caspase 3, Bax, p-p38, and p38 were measured using western blot. Luciferase reporter assay and RNA immunoprecipitation assay were applied to ensure that miR-399-3p targeted TRAF3. Caerulein promoted the expression of TNF-α, IL-1β, and IL-6, enhanced the expression of C-caspase 3 and Bax while inhibited Bcl-2 protein expression. Meanwhile, caerulein also reduced the expression of miR-339-3p and induced the expression of TRAF3 in rat pancreatic acinar cells. miR-399-3p transfection inhibited the levels of TNF-α, IL-1β, and IL-6 and C-caspase 3 and Bax protein expression as well as suppressed cell apoptosis, while increased Bcl-2 protein expression in caerulein-induced AP. TRAF3 has been verified as a target of miR-339-3p. Interestingly, the reduction of miR-399-3p inhibited the p38 pathway, which was impaired by the upregulation of TRAF3. In addition, the suppression effects of miR-339-3p on cell inflammation and apoptosis in caerulein-induced AP were reversed by enhancing TRAF3 expression. In this study, in vitro model of AP was characterized by strong inflammation and cell apoptosis. We have first demonstrated the regulatory network of miR-339-3p and TRAF3. Overexpression of miR-339-3p inhibited cell inflammation and cell apoptosis in caerulein-induced AP through modulating TRAF3 expression via the p38 pathway, providing a new therapeutic target in the treatment of AP.

scholarly journals Expression and possible role of Smad3 in postnecrotizing enterocolitis stricture

2022 ◽  
Vol 5 (1) ◽  
pp. e000289
Author(s):  
Rui Chen ◽  
Chengjie Lv ◽  
Xiaoxia Zhao ◽  
Dong Ma ◽  
Dengming Lai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Cell Proliferation And Migration ◽  
Tnf Α ◽  
Protein Expressions ◽  
Smad3 Protein ◽  
And Migration ◽  
Emt Markers ◽  
Tgf Β1 ◽  
Proliferation And Migration

ObjectiveTo investigate the expression of Smad3 (mothers against decapentaplegic homolog 3) protein in postnecrotizing enterocolitis stricture and its possible mechanism of action.MethodsWe used immunohistochemistry to detect the expression characteristics of Smad3 and nuclear factor kappa B (NF-κB) proteins in human postnecrotizing enterocolitis stricture. We cultured IEC-6 (crypt epithelial cells of rat small intestine) in vitro and inhibited the expression of Smad3 using siRNA technique. Quantitative PCR, western blotting, and ELISA were used to detect the changes in transforming growth factor-β1 (TGF-β1), NF-κB, tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), and zonula occludens-1 (ZO-1) messenger RNA (mRNA) and protein expressions in IEC-6 cells. CCK8 kit and Transwell cellular migration were used to detect cell proliferation and migration. Changes in epithelial–mesenchymal transition (EMT) markers (E-cadherin and vimentin) in IEC-6 cells were detected by immunofluorescence technique.ResultsThe results showed that Smad3 protein and NF-κB protein were overexpressed in narrow intestinal tissues and that Smad3 protein expression was positively correlated with NF-κB protein expression. After inhibiting the expression of Smad3 in IEC-6 cells, the mRNA expressions of NF-κB, TGF-β1, ZO-1, and VEGF decreased, whereas the mRNA expression of TNF-α did not significantly change. TGF-β1, NF-κB, and TNF-α protein expressions in IEC-6 cells decreased, whereas ZO-1 and intracellular VEGF protein expressions increased. IEC-6 cell proliferation and migration capacity decreased. There was no significant change in protein expression levels of EMT markers E-cadherin and vimentin and also extracellular VEGF protein expression.ConclusionsWe suspect that the high expression of Smad3 protein in postnecrotizing enterocolitis stricture may promote the occurrence and development of secondary intestinal stenosis. The mechanism may be related to the regulation of TGF-β1, NF-κB, TNF-α, ZO-1, and VEGF mRNA and protein expression. This may also be related to the ability of Smad3 to promote epithelial cell proliferation and migration.

scholarly journals Exosomes derived from circRNA Rtn4-modified BMSCs attenuate TNF-α-induced cytotoxicity and apoptosis in murine MC3T3-E1 cells by sponging miR-146a

2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Guijun Cao ◽  
Xianqing Meng ◽  
Xiaodong Han ◽  
Jinhua Li
Keyword(s):  
Protein Expression ◽  
Cell Viability ◽  
Caspase 3 ◽  
Circular Rna ◽  
Bone Tissue Regeneration ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Bax Protein ◽  
Tnf Α ◽  
Underlying Mechanisms

Abstract Osteoporosis is the most common and complex skeletal disorder worldwide. Exosomes secreted by bone marrow-derived mesenchymal stromal cells (BMSCs) are considered as an ideal seed source for bone tissue regeneration. However, the role of exosomes secreted by BMSCs (BMSCs-Exos) in osteoporosis and its underlying mechanisms remain unclear. In the present study, the expression of microRNA (miRNA)-146a and circular RNA (circRNA) Rtn4 (circ-Rtn4) was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR), and their protein expression was determined by Western blotting. Enzyme-linked immunosorbent assay was performed to detect caspase-3 activity. Cell viability and apoptosis were assessed using 3-(4,5-Dimethylthiazol-2yl-)-2,5-diphenyl tetrazolium bromide (MTT) assay and flow cytometry analysis, respectively. Luciferase reporter assay was exploited for target validation. Results showed that tumor necrosis factor-α (TNF-α) dose-dependently increased miR-146a expression, inhibited cell viability, and promoted cell apoptosis, as indicated by increased caspase-3, cleaved caspase-3, and Bcl-2-associated X protein (Bax) expression as well as caspase-3 activity. However, miR-146a silencing or co-culture with BMSCs-Exos blocked these effects. Moreover, co-culture with exosomes-derived from circ-Rtn4-modified BMSCs (Rtn4-Exos) attenuated TNF-α-induced cytotoxicity and apoptosis in MC3T3-E1 cells, as evidenced by the decrease in caspase-3, cleaved caspase-3, and Bax protein expression and caspase-3 activity. In addition, miR-146a was identified as a target of circ-Rtn4, and Rtn4-Exos exerted their function in TNF-α-treated MC3T3-E1 cells by sponging miR-146a. Hence, our findings suggested that Rtn4-Exos attenuated TNF-α-induced cytotoxicity and apoptosis in murine MC3T3-E1 cells by sponging miR-146a, suggesting that Rtn4-Exos may serve as novel candidates for treating osteoporosis.

scholarly journals Transforming growth factor-β1-regulated Fas/FasL pathway activation suppresses nucleus pulposus cell apoptosis in an inflammatory environment

2020 ◽  
Vol 40 (2) ◽  
Author(s):  
Jingjing Xie ◽  
Bo Li ◽  
Bing Yao ◽  
Pingchao Zhang ◽  
Lixin Wang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Nucleus Pulposus ◽  
Disc Degeneration ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Transforming Growth Factor ◽  
Tnf Α ◽  
Gene And Protein Expression ◽  
Tgf Β1

Abstract Background: During disc degeneration, inflammatory cytokine tumor necrosis factor (TNF)-α is correlated with nucleus pulposus (NP) cell apoptosis. Transforming growth factor (TGF)-β1 has the potential to regenerate degenerative disc. Objective: To investigate the protective role of TGF-β1 against TNF-α-mediated NP cell apoptosis and the underlying mechanism. Methods: Rat NP cells were treated with TNF-α (100 ng/ml) for 48 h. TGF-β1 was added into the culture medium to investigate its protective effects against TNF-α-induced NP cell apoptosis. Exogenous FasL was used to investigate the potential role of the Fas/FasL pathway in this process. Flow cytometry assay was used to analyze NP cell apoptosis. Real-time PCR and Western blotting were used to analyze gene and protein expression of apoptosis-related molecules. Results: In TNF-α-treated NP cells, TGF-β1 significantly decreased NP cell apoptosis, declined caspase-3 and -8 activity, and decreased expression of Bax and caspase-3 (cleaved-caspase-3) but increased expression of Bcl-2. However, exogenous FasL partly reversed these effects of TGF-β1 in NP cells treated with TNF-α. Additionally, expression of Fas and FasL in TNF-α-treated NP cells partly decreased by TGF-β1, whereas exogenous FasL increased expression of Fas and FasL in NP cells treated with TGF-β1 and TNF-α. Conclusion: TGF-β1 helps to inhibit TNF-α-induced NP cell apoptosis and the Fas/FasL pathway may be involved in this process. The present study suggests that TGF-β1 may be effective to retard inflammation-mediated disc degeneration.

scholarly journals Osteogenic protein-1 inhibits nucleus pulposus cell apoptosis through regulating the NF-κB/ROS pathway in an inflammation environment

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Wei Yu ◽  
Jiabin Fu ◽  
Yan Liu ◽  
Yuchi Wu ◽  
Dianming Jiang
Keyword(s):  
Protein Expression ◽  
Disc Degeneration ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Protective Effects ◽  
Transduction Pathway ◽  
Signaling Transduction Pathway ◽  
Tnf Α ◽  
Osteogenic Protein ◽  
Apoptosis Ratio

Background: Intervertebral disc degeneration is a pathological process that involves an inflammation response. As a classical cellular feature, several studies have demonstrated that inflammation can promote nucleus pulposus (NP) cell apoptosis. Therefore, attenuation of NP cell apoptosis may be a potential way to retard disc degeneration. Objective: The present study was aimed to investigate the protective effects of osteogenic protein-1 (OP-1) against NP cell apoptosis in an inflammation environment, and the potential signaling transduction pathway. Methods: Rat NP cells were cultured in medium with or without inflammatory cytokine tumor necrosis factor (TNF)-α for 6 days. The exogenous TNF-α was added into the medium to investigate its protective effects. NP cell apoptosis was evaluated by cell apoptosis ratio, caspase-3 activity, gene/protein expression of apoptosis-related molecules (Bcl-2, Bax, and caspase-3). Additionally, the intracellular reactive oxygen species (ROS) content and activity of the NF-κB pathway were also analyzed. Results: Compared with the control NP cells, TNF-α significantly increased cell apoptosis ratio, caspase-3 activity, gene/protein expression of Bcl-2, Bax and caspase-3, ROS content, and activity of the NF-κB pathway. However, OP-1 partly attenuated these effects in NP cells treated with TNF-α. Conclusion: OP-1 is effective in attenuating TNF-α-caused NP cell apoptosis, and the ROS/NF-κB pathway may be the potential signaling transduction pathway. The present study indicates that OP-1 may be helpful to inhibit inflammation-mediated disc degeneration.

scholarly journals Pearl extract protects HaCaT cells from UV radiation-induced apoptosis through mitochondrial pathway regulation

2020 ◽  
Author(s):  
Zhixiong Chen ◽  
jing wang ◽  
Anquan Yang ◽  
Lihua Zhang ◽  
Yaojia Lu ◽  
...  
Keyword(s):  
Protein Expression ◽  
Caspase 3 ◽  
Hacat Cells ◽  
Caspase 9 ◽  
Expression Levels ◽  
Protein Levels ◽  
Bax Protein ◽  
Reactive Oxygen Species Content ◽  
Tnf Α ◽  
Induced Apoptosis

Abstract Background: Previous studies have demonstrated that pearl extract (PE) promotes wound healing and skin whitening. However, it remains unclear whether PE can inhibit ultraviolet (UV)-photodamage in HaCaT cells. In this study, an in vitro photoaging cell model was established to observe the effect of PE on UV-induced damage and the apoptosis of HaCaT cells. The aim of this study was to provide a reference for the future development of natural sunscreens.Results: PE concentrations of 0.1 and 1 μg/mL were considered the most effective and safe concentrations. Compared to that in the control group, superoxide dismutase and glutathione peroxidase activity in the photoaging group was significantly reduced, whereas malondialdehyde and reactive oxygen species content, along with tumour necrosis factor-alpha (TNF-α) and interleukin (IL)-10 mRNA and protein levels, were markedly increased. In contrast, Bcl-2 protein expression was significantly decreased, whereas caspase-3, caspase-9, and Bax protein expression levels were significantly increased. Compared to that in the photoaging group, HaCaT cell proliferation was significantly increased in the PE group. Both PE concentrations significantly increased superoxide dismutase and glutathione peroxidase activity in cells, reduced malondialdehyde and reactive oxygen species content, decreased TNF-α and IL-10 mRNA expression in cells, and reduced TNF-α and IL-10 protein levels in the supernatant. Additionally, Bcl-2 protein expression levels were significantly increased, whereas caspase-3, caspase-9, and Bax protein expression levels were significantly reduced by PE treatment.Conclusions: PE can inhibit UV-induced apoptosis by inhibiting mitochondria-mediated apoptosis and regulating TNF-α and IL-10 expression.

scholarly journals LncRNA UCA1 promotes development of gastric cancer via the miR-145/MYO6 axis

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
An Yang ◽  
Xin Liu ◽  
Ping Liu ◽  
Yunzhang Feng ◽  
Hongbo Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Lines ◽  
Development Of Gastric Cancer

Abstract Background Long noncoding RNA (lncRNA), urothelial carcinoma-associated 1 (UCA1) is aberrantly expressed in multiple cancers and has been verified as an oncogene. However, the underlying mechanism of UCA1 in the development of gastric cancer is not fully understood. In the present study, we aimed to identify how UCA1 promotes gastric cancer development. Methods The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) data were used to analyze UCA1 and myosin VI (MYO6) expression in gastric cancer. Western blot and quantitative real-time PCR (QPCR) were performed to test the expression level of the UCA1/miR-145/MYO6 axis in gastric cancer cell lines and tissues. The roles of the UCA1/miR-145/MYO6 axis in gastric cancer in vitro and in vivo were investigated by CCK-8 assay, flow cytometry, siRNAs, immunohistochemistry, and a mouse xenograft model. The targeted relationship among UCA1, miR-145, and MYO6 was predicted using LncBase Predicted v.2 and TargetScan online software, and then verified by luciferase activity assay and RNA immunoprecipitation. Results UCA1 expression was higher but miR-145 expression was lower in gastric cancer cell lines or tissues, compared to the adjacent normal cell line or normal tissues. Function analysis verified that UCA1 promoted cell proliferation and inhibited cell apoptosis in the gastric cancer cells in vitro and in vivo. Mechanistically, UCA1 could bind directly to miR-145, and MYO6 was found to be a downstream target gene of miR-145. miR-145 mimics or MYO6 siRNAs could partly reverse the effect of UCA1 on gastric cancer cells. Conclusions UCA1 accelerated cell proliferation and inhibited cell apoptosis through sponging miR-145 to upregulate MYO6 expression in gastric cancer, indicating that the UCA1/miR-145/MYO6 axis may serve as a potential therapeutic target for gastric cancer.

scholarly journals Pirfenidone attenuates synovial fibrosis and postpones the progression of osteoarthritis by anti-fibrotic and anti-inflammatory properties in vivo and in vitro

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Qilu Wei ◽  
Ning Kong ◽  
Xiaohui Liu ◽  
Run Tian ◽  
Ming Jiao ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Fast Green ◽  
Expression Levels ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Safranin O ◽  
Tgf Β1

Abstract Background Osteoarthritis (OA) is a disease of the entire joint involving synovial fibrosis and inflammation. Pathological changes to the synovium can accelerate the progression of OA. Pirfenidone (PFD) is a potent anti-fibrotic drug with additional anti-inflammatory properties. However, the influence of PFD on OA is unknown. Methods Proliferation of human fibroblast-like synoviocytes (FLSs) after treatment with TGF-β1 or PFD was evaluated using a Cell Counting Kit-8 assay and their migration using a Transwell assay. The expression of fibrosis-related genes (COL1A1, TIMP-1, and ACTA-2) and those related to inflammation (IL-6 and TNF-α) was quantified by real-time quantitative PCR. The protein expression levels of COL1A1, α-SMA (coded by ACTA-2), IL-6 and TNF-α were measured by enzyme-linked immunosorbent assay. A rabbit model of OA was established and then PFD was administered by gavage. The expression of genes related to fibrosis (COL1A1, TIMP-1, and ADAM-12) and inflammation (IL-6 and TNF-α) was measured using RNA extracted from the synovium. Synovial tissue was examined histologically after staining with H&E, Masson’s trichrome, and immunofluorescence. Synovitis scores, the volume fraction of collagen, and mean fluorescence intensity were calculated. Degeneration of articular cartilage was analyzed using a Safranin O-fast green stain and OARSI grading. Results The proliferation of FLSs was greatest when induced with 2.5 ng/ml TGF-β1 although it did not promote their migration. Therefore, 2.5 ng/ml TGF-β1 was used to stimulate the FLSs and evaluate the effects of PFD, which inhibited the migration of FLSs at concentrations as low as 1.0 mg/ml. PFD decreased the expression of COL1A1 while TGF-β1 increased both mRNA and protein expression levels of IL-6 but had no effect on α-SMA or TNF-α expression. PFD decreased mRNA expression levels of COL1A1, IL-6, and TNF-α in vivo. H&E staining and synovitis scores indicated that PFD reduced synovial inflammation, while Masson’s trichrome and immunofluorescence staining suggested that PFD decreased synovial fibrosis. Safranin O-Fast Green staining and the OARSI scores demonstrated that PFD delayed the progression of OA. Conclusions PFD attenuated synovial fibrosis and inflammation, and postponed the progression of osteoarthritis in a modified Hulth model of OA in rabbits, which was related to its anti-fibrotic and anti-inflammatory properties.

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