scholarly journals Bugan Rongjin decoction alleviates inflammation and oxidative stress to treat the postmenopausal knee osteoarthritis through Wnt signaling pathway

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Sheng Wang ◽  
Pei Ding ◽  
Xiaopeng Xia ◽  
Xuexian Chen ◽  
Daguo Mi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Knee Osteoarthritis ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Wnt Signaling Pathway ◽  
Cartilage Tissue ◽  
Ovx Rats ◽  
And Oxidative Stress

Abstract Background Traditional Chinese medicine has been found effective for the therapy of knee osteoarthritis (KOA). This study was aimed at investigating the underlying mechanism of Bugan Rongjin decoction (BGRJ) in treating the postmenopausal KOA. Results Ovariectomized rat model of KOA and LPS-induced chondrocytes were successfully constructed for in vivo and in vitro model of postmenopausal KOA. X-ray and hematoxylin–eosin (H&E) staining showed that BGRJ alleviated pathological damage of articular cartilage in OVX rats with KOA. In addition, BGRJ inhibited inflammation and oxidative stress through decreasing the levels of serum IL-6, IL-1β, TNF-α and NO and regulated Wnt signaling pathway by downregulating the expression of Wnt5a and β-catenin and upregulating the expression of Sox9 and Collagen II in cartilage tissue, detected by immunohistochemistry (IHC) and western blot analysis. Furthermore, Wnt5a silencing reduced the apoptosis of LPS-induced ADTC5 cells, which was further suppressed by the combination of downregulation of Wnt5a and BGRJ. Conclusions In summary, BGRJ alleviates inflammation and oxidative stress to treat the postmenopausal KOA through Wnt signaling pathway.

scholarly journals Dickkopf Wnt signaling pathway inhibitor 1 regulates the differentiation of mouse embryonic stem cells in vitro and in vivo

2015 ◽  
Vol 13 (1) ◽  
pp. 720-730 ◽  
Author(s):  
LIPING OU ◽  
LIAOQIONG FANG ◽  
HEJING TANG ◽  
HAI QIAO ◽  
XIAOMEI ZHANG ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Wnt Signaling Pathway ◽  
Embryonic Stem ◽  
Mouse Embryonic Stem Cells

scholarly journals Modulation of Calretinin Expression in Human Mesothelioma Cells Reveals the Implication of the FAK and Wnt Signaling Pathways in Conferring Chemoresistance towards Cisplatin

2019 ◽  
Vol 20 (21) ◽  
pp. 5391 ◽  
Author(s):  
Wörthmüller ◽  
Salicio ◽  
Oberson ◽  
Blum ◽  
Schwaller
Keyword(s):  
Wnt Signaling ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Expression System ◽  
Single Agent ◽  
Wnt Signaling Pathway ◽  
Tumor Formation ◽  
Mesenchymal Transition

Malignant mesothelioma (MM) is an aggressive asbestos-linked neoplasm, characterized by dysregulation of signaling pathways. Due to intrinsic or acquired chemoresistance, MM treatment options remain limited. Calretinin is a Ca2+-binding protein expressed during MM tumorigenesis that activates the FAK signaling pathway, promoting invasion and epithelial-to-mesenchymal transition. Constitutive calretinin downregulation decreases MM cells’ growth and survival, and impairs tumor formation in vivo. In order to evaluate early molecular events occurring during calretinin downregulation, we generated a tightly controlled IPTG-inducible expression system to modulate calretinin levels in vitro. Calretinin downregulation significantly reduced viability and proliferation of MM cells, attenuated FAK signaling and reduced the invasive phenotype of surviving cells. Importantly, surviving cells showed a higher resistance to cisplatin due to increased Wnt signaling. This resistance was abrogated by the Wnt signaling pathway inhibitor 3289-8625. In various MM cell lines and regardless of calretinin expression levels, blocking of FAK signaling activated the Wnt signaling pathway and vice versa. Thus, blocking both pathways had the strongest impact on MM cell proliferation and survival. Chemoresistance mechanisms in MM cells have resulted in a failure of single-agent therapies. Targeting of multiple components of key signaling pathways, including Wnt signaling, might be the future method-of-choice to treat MM.

scholarly journals The endocannabinoid anandamide inhibits cholangiocarcinoma growth via activation of the noncanonical Wnt signaling pathway

2008 ◽  
Vol 295 (6) ◽  
pp. G1150-G1158 ◽  
Author(s):  
Sharon DeMorrow ◽  
Heather Francis ◽  
Eugenio Gaudio ◽  
Julie Venter ◽  
Antonio Franchitto ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Growth ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Calcium Release ◽  
Wnt Signaling Pathway ◽  
Xenograft Model ◽  
Orphan Receptor

Cholangiocarcinomas are cancers that have poor prognosis and limited treatment options. The noncanonical Wnt pathway is mediated predominantly by Wnt 5a, which activates a Ca2+-dependent pathway involving protein kinase C, or a Ca2+-independent pathway involving the orphan receptor Ror2 and subsequent activation of Jun NH2-terminal kinase (JNK). This pathway is associated with growth-suppressing effects in numerous cell types. We have shown that anandamide decreases cholangiocarcinoma growth in vitro. Therefore, we determined the effects of anandamide on cholangiocarcinoma tumor growth in vivo using a xenograft model and evaluated the effects of anandamide on the noncanonical Wnt signaling pathways. Chronic administration of anandamide decreased tumor growth and was associated with increased Wnt 5a expression in vitro and in vivo. Treatment of cholangiocarcinoma cells with recombinant Wnt 5a decreased cell proliferation in vitro. Neither anandamide nor Wnt 5a affected intracellular calcium release, but both increased the JNK phosphorylation. Stable knockdown of Wnt 5a or Ror2 expression in cholangiocarcinoma cells abolished the effects of anandamide on cell proliferation and JNK activation. Modulation of the endocannabinoid system may be important in cholangiocarcinoma treatment. The antiproliferative actions of the noncanonical Wnt signaling pathway warrants further investigation to dissect the mechanism by which this may occur.

scholarly journals Krüppel-Like Factor 6 Silencing Prevents Oxidative Stress and Neurological Dysfunction Following Intracerebral Hemorrhage via Sirtuin 5/Nrf2/HO-1 Axis

2021 ◽  
Vol 13 ◽  
Author(s):  
Jia Sun ◽  
Jinzhong Cai ◽  
Junhui Chen ◽  
Siqiaozhi Li ◽  
Xin Liao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intracerebral Hemorrhage ◽  
Signaling Pathway ◽  
Hippocampal Neurons ◽  
Neuronal Apoptosis ◽  
Neurological Dysfunction ◽  
Heme Oxygenase 1 ◽  
And Oxidative Stress

As a severe neurological deficit, intracerebral hemorrhage (ICH) is associated with overwhelming mortality. Subsequent oxidative stress and neurological dysfunction are likely to cause secondary brain injury. Therefore, this study sought to define the role of Krüppel-like factor 6 (KLF6) and underlying mechanism in oxidative stress and neurological dysfunction following ICH. An in vivo model of ICH was established in rats by injection of autologous blood, and an in vitro ICH cell model was developed in hippocampal neurons by oxyhemoglobin (OxyHb) exposure. Next, gain- and loss-of-function assays were performed in vivo and in vitro to clarify the effect of KLF6 on neurological dysfunction and oxidative stress in ICH rats and neuronal apoptosis and mitochondrial reactive oxygen species in OxyHb-induced hippocampal neurons. KLF6, nuclear factor erythroid 2–related factor 2 (Nrf2), and heme oxygenase 1 (HO-1) were highly expressed in hippocampal tissues of ICH rats, whereas sirtuin 5 (SIRT5) presented a poor expression. Mechanistically, KLF6 bound to the SIRT5 promoter and transcriptionally repressed SIRT5 to activate the Nrf2/HO-1 signaling pathway. KLF6 silencing alleviated neurological dysfunction and oxidative stress in ICH rats and diminished oxidative stress and neuronal apoptosis in OxyHb-induced neurons, whereas SIRT5 overexpression negated its effect. To sum up, KLF6 silencing elevated SIRT5 expression to inactivate the Nrf2/HO-1 signaling pathway, thus attenuating oxidative stress and neurological dysfunction after ICH.

Ellagic Acid Attenuates BLM-Induced Pulmonary Fibrosis via Inhibiting Wnt Signaling Pathway

2020 ◽  
Author(s):  
Xiaohe Li ◽  
kai huang ◽  
Xiaowei Liu ◽  
Hao Ruan ◽  
Ling Ma ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Ellagic Acid ◽  
Cell Damage ◽  
Wnt Signaling Pathway ◽  
Pharmacological Activities ◽  
Natural Polyphenol

Abstract Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with high mortality, which characterized by epithelial cell damage and fibroblasts activation. Ellagic acid (EA) is a natural polyphenol compound widely found in fruits and nuts which has demonstrated multiple pharmacological activities. Herein we showed that Ellagic acid significantly alleviated bleomycin(BLM)-induced pulmonary fibrosis in mice, and also inhibited the Wnt/β-catenin signal in primary pulmonary fibroblasts. In vitro experiments indicated that Ellagic acid apparently suppressed Wnt3a-induced myofibroblasts activation and ECM accumulation mainly via inhibiting the phosphorylation of Erk2 and Akt. Further studies showed that Ellagic acid could induce autophagy formation of myofibroblasts mainly by suppressing mTOR signaling and promote apoptosis of myofibroblasts. In vivo experiments reveled that Ellagic acid significantly inhibited myofibroblasts activation and promoted autophagy formation. Taken together, our results showed that Ellagic acid effectively attenuated BLM-induced pulmonary fibrosis in mice by suppressing myofibroblasts activation, promoting autophagy and apoptosis of myofibroblasts mainly via inhibiting Wnt signaling pathway.

scholarly journals Bisphenol-A exposure alters memory consolidation and hippocampal CA1 spine formation through Wnt signaling in vivo and in vitro

2015 ◽  
Vol 4 (3) ◽  
pp. 686-694 ◽  
Author(s):  
Zhi-Hua Liu ◽  
Ye Yang ◽  
Meng-Meng Ge ◽  
Li Xu ◽  
Yuqing Tang ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Memory Consolidation ◽  
Wnt Signaling Pathway ◽  
Spine Formation ◽  
Hippocampal Ca1

Based on Wnt signaling pathway, this study aims to further mechanistically understand memory alteration after BPA exposure.

scholarly journals The Novel Tumor Suppressor Gene ZNF24 Induces THCA Cells Senescence by Regulating Wnt Signaling Pathway, Resulting in Inhibition of THCA Tumorigenesis and Invasion

2021 ◽  
Vol 11 ◽  
Author(s):  
Juan Xiong ◽  
Panpan Jiang ◽  
Li Zhong ◽  
Youling Wang
Keyword(s):  
Tumor Suppressor ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Nude Mice ◽  
Treatment Options ◽  
Ectopic Expression ◽  
Wnt Signaling Pathway ◽  
Migration And Invasion

ObjectClinically, the effective treatment options available to thyroid cancer (THCA) patients are very limited. Elucidating the features of tumor suppressor genes (TSGs) and the corresponding signal transduction cascade may provide clues for the development of new strategies for targeted therapy of THCA. Therefore, this paper aims to explore the mechanism of ZNF24 underlying promoting THCA cell senescence at molecular level.MethodsWe performed RT-PCR and Western Blotting for evaluating associated RNA and protein expression. CCK8, colony forming, wound healing and Transwell chamber assays were conducted to examine THCA cell proliferation, invasion and migration. β-galactosidase staining assay was performed to detect THCA cells senescence. The size and volume of xenotransplanted tumors in nude mice are calculated to asses ZNF24 effect in vivo.ResultsEctopic expression of ZNF24 significantly inhibited the cell viability, colony forming, migration and invasion abilities of THCA cell lines (K1/GLAG-66i and BCPAPi) (P < 0.05). ZNF24 induced BCPAPi cells senescence through regulating Wnt signaling pathway. ZNF24 inhibited Wnt signaling pathway activition by competitively binding β-catenin from LEF1/TCF1-β-catenin complex. In nude mice, both Ectopic expression of ZNF24 and 2,4-Da (the strong β-catenin/Tcf-4 inhibitor) treatment significantly decreased both the size and weight of xenotransplanted tumors when compared with control mice (P < 0.05).ConclusionResults obtained in vivo and in vitro reveal the role of ZNF24 in significantly suppressing THCA tumorigenesis and invasion by regulating Wnt signaling pathway.

scholarly journals Tanreqing Inhibits LPS-Induced Acute Lung Injury In Vivo and In Vitro Through Downregulating STING Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Yu-Qiong He ◽  
Can-Can Zhou ◽  
Jiu-Ling Deng ◽  
Liang Wang ◽  
Wan-Sheng Chen
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Signaling Pathway ◽  
Inflammatory Responses ◽  
Lung Edema ◽  
Protective Effects ◽  
And Oxidative Stress

Acute lung injury (ALI) is a common life-threatening lung disease, which is mostly associated with severe inflammatory responses and oxidative stress. Tanreqing injection (TRQ), a Chinese patent medicine, is clinically used for respiratory-related diseases. However, the effects and action mechanism of TRQ on ALI are still unclear. Recently, STING as a cytoplasmic DNA sensor has been found to be related to the progress of ALI. Here, we showed that TRQ significantly inhibited LPS-induced lung histological change, lung edema, and inflammatory cell infiltration. Moreover, TRQ markedly reduced inflammatory mediators release (TNF-α, IL-6, IL-1β, and IFN-β). Furthermore, TRQ also alleviated oxidative stress, manifested by increased SOD and GSH activities and decreased 4-HNE, MDA, LDH, and ROS activities. In addition, we further found that TRQ significantly prevented cGAS, STING, P-TBK, P-P65, P-IRF3, and P-IκBα expression in ALI mice. And we also confirmed that TRQ could inhibit mtDNA release and suppress signaling pathway mediated by STING in vitro. Importantly, the addition of STING agonist DMXAA dramatically abolished the protective effects of TRQ. Taken together, this study indicated that TRQ alleviated LPS-induced ALI and inhibited inflammatory responses and oxidative stress through STING signaling pathway.

Long Noncoding RNA Maternally Expressed Gene 3 Targets miR-30b and Regulates the AKT Serine/Threonine Kinase 1/Phosphoinositide 3-Kinase Signaling Pathway of H2O2-Induced Proliferation, Apoptosis, and Oxidative Stress in Retinal Ganglion Cells

2021 ◽  
Vol 11 (3) ◽  
pp. 351-358
Author(s):  
Kai Yan ◽  
Lin Niu ◽  
Huili Tian ◽  
Fanfan Su ◽  
Yao Chen
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Noncoding Rna ◽  
Retinal Ganglion ◽  
Pi3k Signaling Pathway ◽  
Related Proteins ◽  
And Oxidative Stress ◽  
Maternally Expressed Gene 3

Oxidative stress is an important factor affecting retinal ganglion cell (RGC) apoptosis. RGC apoptosis is the main pathophysiological feature of visual impairment as a result of glaucoma. Recently, it has been found that long noncoding RNA (lncRNA) and microRNAs are involved in RGC apoptosis. Here, the function of lncRNA maternally expressed gene 3 (MEG3) and miR-30b in H2 O2-induced RGC proliferation, apoptosis, and oxidative stress was investigated. The expression levels of MEG3 and miR-30b were detected by RT-PCR; the effects of MEG3 and miR-30b on the proliferation and apoptosis of RGCs were observed by flow cytometry; the levels of apoptosis-related proteins and AKT/PI3K signal pathway proteins were detected by protein immunoassay; and the regulation of miR-34a by pvt1 was verified by in vivo and in vitro experiments. The expression of MEG3 and miR-30b increased and decreased significantly in RGCs treated by H2O2. MEG3 expression decreased, apoptosis level-related proteins decreased, the apoptosis rate reduced, and the activity of MDA and SOD decreased. When the expression of miR-34a was inhibited, the proliferation rate of RGCs increased, the apoptosis rate decreased, and the level of apoptosis-related proteins decreased, which reversed MEG3’s effect on RGC apoptosis and proliferation. Furthermore, pvt1 could bind the miR-30b promoter and regulate it with in vitro expression and in vivo expression. Besides, we found that miR-30b can regulate the AKT/PI3K signaling pathway and participate in cell apoptosis and hyperplasia in stress response. LncRNA MEG3 targets miR-30b and regulates the AKT/PI3K signaling pathway on H2 O2-induced cell apoptosis, hyperplasia, and oxidative stress of RGCs.

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