Wnt5a/Platelet‐rich plasma synergistically inhibits IL‐1β‐induced inflammatory activity through NF‐κB signaling pathway and prevents cartilage damage and promotes meniscus regeneration

2021 ◽  
Author(s):  
Yiying Qi ◽  
Ruofu Tang ◽  
Zuobing Shi ◽  
Gang Feng ◽  
Wenkan Zhang
Keyword(s):  
Signaling Pathway ◽  
Platelet Rich Plasma ◽  
Cartilage Damage ◽  
Inflammatory Activity ◽  
Meniscus Regeneration

AB0070 Wnt and wisp1 expression in the synovium induces cartilage damage by skewing of tgf-beta signaling via the canonical wnt signaling pathway

2013 ◽  
Vol 72 (Suppl 3) ◽  
pp. A807.1-A807
Author(s):  
M. H. van den Bosch ◽  
A. B. Blom ◽  
P. L. van Lent ◽  
H. M. van Beuningen ◽  
F. A. van de Loo ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Signaling Pathway ◽  
Cartilage Damage ◽  
Wnt Signaling Pathway ◽  
Tgf Beta ◽  
Canonical Wnt Signaling ◽  
Canonical Wnt

Archidendron lucidum Exerts Anti-Inflammatory Effects by Targeting PDK1 in the NF-κB Pathway

2020 ◽  
Vol 48 (02) ◽  
pp. 429-444
Author(s):  
Minkyeong Jo ◽  
Young-Su Yi ◽  
Jae Youl Cho
Keyword(s):  
Signaling Pathway ◽  
Hplc Analysis ◽  
Inflammatory Diseases ◽  
Interleukin 1 ◽  
Inflammatory Activity ◽  
Raw264.7 Cells ◽  
Luciferase Reporter ◽  
No Production ◽  
Pharmacological Activities ◽  
Anti Inflammatory

Pharmacological activities of some Leguminosae family members were reported. Pharmacological activities of Archidendron lucidum, a Leguminosae family member have never been explored. Therefore, this study investigated anti-inflammatory effects of an Archidendron lucidum methanol extract (Al-ME). In this study, anti-inflammatory effects of Al-ME were investigated in LPS-stimulated RAW264.7 cells and HCl/EtOH-induced gastritis mice by MTT assay, nitric oxide (NO) production assay, semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), luciferase reporter assay, and Western blotting. High-performance liquid chromatography (HPLC) analysis identified ethnopharmacological compounds in Al-ME. Al-ME inhibited NO production without cytotoxicity in peritoneal macrophages and RAW264.7 cells stimulated with LPS or Pam3CSK4. Al-ME downregulated mRNA expression of inflammatory genes (inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2)) and pro-inflammatory cytokines (tumor necrosis factor-[Formula: see text] (TNF-[Formula: see text]), interleukin-1[Formula: see text] (IL-1[Formula: see text]), and IL-6). Al-ME exerted anti-inflammatory activity in LPS-stimulated RAW264.7 cells by inhibiting nuclear factor-kappa B (NF-[Formula: see text]B) signaling pathway. HPLC analysis identified quercetin, luteolin, and kaempferol as major anti-inflammatory components in Al-ME. Al-ME ameliorated HCl/EtOH-induced gastritis symptoms in mice by suppressing iNOS and IL-6 mRNA expressions and I[Formula: see text]B[Formula: see text] phosphorylation. Therefore, these results suggest that Al-ME exhibited anti-inflammatory activity by targeting NF-[Formula: see text]B signaling pathway, implying that Al-ME could be potent anti-inflammatory medications to prevent and treat inflammatory diseases.

scholarly journals Platelet-Rich Plasma with Endothelial Progenitor Cells Accelerates Diabetic Wound Healing in Rats by Upregulating the Notch1 Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Cheng Zhang ◽  
Yu Zhu ◽  
Shengdi Lu ◽  
Wanrun Zhong ◽  
Yanmao Wang ◽  
...  
Keyword(s):  
Wound Healing ◽  
Growth Factors ◽  
Signaling Pathway ◽  
Platelet Rich Plasma ◽  
Diabetic Wound ◽  
Endothelial Progenitor ◽  
Notch1 Signaling ◽  
Diabetic Wound Healing ◽  
Notch1 Signaling Pathway ◽  
Diabetic Wounds

Diabetic wounds, as a kind of refractory wound, are very difficult to heal. Both endothelial progenitor cell (EPC) transplantation and platelet-rich plasma (PRP) can improve diabetic wound healing to some extent. However, PRP application cannot provide reparative cells, while EPC transplantation cannot replenish the required growth factors for wound healing. Thus, when applied alone, neither of these factors is sufficient for effective wound healing. Furthermore, the proliferation, differentiation, and fate of the transplanted EPCs are not well known. Therefore, in this study, we examined the efficacy of combined PRP application with EPC transplantation in diabetic wound healing. Our results indicated that PRP application improved EPC proliferation and migration. The Notch signaling pathway plays a key role in the regulation of the proliferation and differentiation of stem cells and angiogenesis in wound healing. The application of PRP upregulated the Notch pathway-related gene and protein expression in EPCs. Furthermore, experiments with shNotch1-transfected EPCs indicated that PRP enhanced the function of EPCs by upregulating the Notch1 signaling pathway. In vivo studies further indicated that the combination of PRP and EPC transplantation increased neovascularization, reduced wound size, and improved healing in rat wound models. Thus, PRP application can provide the necessary growth factors for wound healing, while EPC transplantation offers the required cells, indicating that the combination of both is a potent novel approach for treating diabetic wounds.

Ethanol Extract of Lilium Bulbs Plays an Anti-Inflammatory Role by Targeting the IKKα/β-Mediated NF-κB Pathway in Macrophages

2018 ◽  
Vol 46 (06) ◽  
pp. 1281-1296 ◽  
Author(s):  
Sang Yun Han ◽  
Young-Su Yi ◽  
Seong-Gu Jeong ◽  
Yo Han Hong ◽  
Kang Jun Choi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Inflammatory Responses ◽  
Inflammatory Activity ◽  
Raw264.7 Cells ◽  
No Production ◽  
Dependent Manner ◽  
Bioactive Components ◽  
Anti Inflammatory

Lilium bulbs have long been used as Chinese traditional medicines to alleviate the symptoms of various human inflammatory diseases. However, mechanisms of Lilium bulb-mediated anti-inflammatory activity and the bioactive components in Lilium bulbs remain unknown. In the present study, the anti-inflammatory activity of Lilium bulbs and the underlying mechanism of action were investigated in macrophages using Lilium bulb ethanol extracts (Lb-EE). In a dose-dependent manner, Lb-EE inhibited nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated RAW264.7 cells and bone marrow-derived macrophages (BMDMs) without causing significant cytotoxicity. Lb-EE also down-regulated mRNA expression of inflammatory genes in LPS-stimulated RAW264.7 cells, which included inducuble nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), and tumor necrosis factor-[Formula: see text] (TNF-[Formula: see text]). Furthermore, Lb-EE markedly restored LPS-induced morphological changes in RAW264.7 cells to a normal morphology. HPLC analysis identified quercetin, luteolin, and kaempferol as bioactive components contained in Lb-EE. Mechanistic studies in LPS-stimulated RAW264.7 cells revealed that Lb-EE suppressed MyD88- and TRIF-induced NF-[Formula: see text]B transcriptional activation and the nuclear translocation of NF-[Formula: see text]B transcription factors. Moreover, Lb-EE inhibited IKK[Formula: see text]/[Formula: see text]-induced activation of the NF-[Formula: see text]B signaling pathway and IKK inhibition significantly reduced NO production in LPS-stimulated RAW264.7 cells. Taken together, these results suggest that Lb-EE plays an anti-inflammatory role by targeting IKK[Formula: see text]/[Formula: see text]-mediated activation of the NF-[Formula: see text]B signaling pathway during macrophage-mediated inflammatory responses.

scholarly journals Higenamine inhibits IL-1β-induced inflammation in human nucleus pulposus cells

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Xiaoliang Bai ◽  
Wenyuan Ding ◽  
Sidong Yang ◽  
Xiaohui Guo
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Nucleus Pulposus ◽  
Inflammatory Activity ◽  
Nucleus Pulposus Cells ◽  
Necrosis Factor Alpha ◽  
Natural Progression ◽  
Anti Inflammatory ◽  
Inflammatory Molecules ◽  
Oxide Synthase

Abstract Intervertebral disc degeneration (IDD) is a natural progression of the aging process associated with inflammation. Higenamine, a plant-based alkaloid, has been identified to possess various pharmacological properties, including anti-inflammatory activity. In the present study, we aimed to evaluate the role of higenamine in interleukin (IL)-1β-induced inflammation in human nucleus pulposus cells (NPCs). The results showed that higenamine improved cell viability in IL-1β-induced NPCs. The IL-1β-dependent up-regulation of inflammatory molecules including inducible nitric oxide synthase (iNOS), nitric oxide (NO), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), tumor necrosis factor alpha (TNF-α), and IL-6 was attenuated by higenamine in NPCs. The increased productions of matrix metalloproteinases (MMP-3 and MMP-13), as well as a disintegrin and metalloprotease with thrombospondin motifs (ADAMTS-4 and ADAMTS-5) were significantly mitigated by higenamine treatment. Furthermore, we also found that higenamine suppressed the IL-1β-induced activation of NF-κB signaling pathway in NPCs. In conclusion, the present study proved that higenamine exhibited anti-inflammatory activity against IL-1β-induced inflammation in NPCs via inhibiting NF-κB signaling pathway. These results suggested that higenamine might be a therapeutic agent for the treatment of IDD.

Stromal Vascular Fraction and Platelet-Rich Plasma Upregulate Vascular Endothelial Growth Factor Expression to Promote Hair Growth via the Wnt/β-Catenin Signaling Pathway

2019 ◽  
Vol 11 (12) ◽  
pp. 1685-1692
Author(s):  
Yarui Liu ◽  
Jindou Jiang ◽  
Yuan Ye ◽  
Zhehao Li ◽  
Meijun Tan ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Hair Follicle ◽  
Signaling Pathway ◽  
Hair Growth ◽  
Platelet Rich Plasma ◽  
Stromal Vascular Fraction ◽  
Follicle Cells ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Androgenetic alopecia (AGA) is a hair loss disease. At present, use of the stromal vascular fraction (SVF) and platelet-rich plasma (PRP) are thought to be the novel, safe, and effective treatment options of AGA, but the mechanism by which SVF and PRP promote hair growth is unclear. Here, we investigated the mechanism underlying the effects of SVF and PRP on hair growth by in vitro culture and in vivo modeling. SVF and PRP promoted hair growth, as was evident from the observation and counting of hair on the back skin of nude mice using ImageJ software. SVF and PRP promoted hair growth, and SVF worked better. We performed nucleic acid extraction with nanomagnetic beads, and the protein levels were extracted with a bicinchoninic acid protein assay kit. The results of western blot analysis and quantitative polymerase chain reaction (qPCR) showed that both SVF and PRP promoted the expression of anti-apoptotic genes. The effect of SVF was better than that of PRP. The results of EdU and hematoxylin and eosin staining showed that SVF and PRP induced the proliferation of hair follicle cells. SVF exerted better effects on the proliferation of hair follicle cells than PRP. Enzyme-linked immunosorbent assay (ELISA) results showed that the expression of the proteins associated with the Wnt/β-catenin process, including vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), alkaline phosphatase (ALP), Wnt10b, and β-catenin, significantly increased in the SVF-treated and PRP-treated dermal/epidermal cells as compared with the control cells. Therefore, SVF and PRP increased the expression of VEGF and PDGF through the Wnt/β-catenin signaling pathway to promote hair growth. The effect of SVF on dermal cells/epidermal cells was stronger than that of PRP, and the difference was statistically significant (P < 0.05).

Anti-inflammatory activity of flavonoids in Nepalese propolis is attributed to inhibition of the IL-33 signaling pathway

2015 ◽  
Vol 25 (1) ◽  
pp. 189-198 ◽  
Author(s):  
Megumi Funakoshi-Tago ◽  
Kazuhi Okamoto ◽  
Rika Izumi ◽  
Kenji Tago ◽  
Ken Yanagisawa ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Inflammatory Activity ◽  
Anti Inflammatory

Puerarin Attenuates Osteoarthritis via Upregulating AMP-Activated Protein Kinase/Proliferator-Activated Receptor-γ Coactivator-1 Signaling Pathway in Osteoarthritis Rats

Pharmacology ◽  
2018 ◽  
Vol 102 (3-4) ◽  
pp. 117-125 ◽  
Author(s):  
Luyao Wang ◽  
Haojie Shan ◽  
Bin Wang ◽  
Nan Wang ◽  
Zubin Zhou ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Signaling Pathway ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Cartilage Damage ◽  
Joint Disease ◽  
Mitochondrial Dysfunctions ◽  
Compound C ◽  
Amp Activated Protein Kinase ◽  
And Cartilage

Background/Aims: Osteoarthritis is the most common degenerative joint disease and causes major pain and disability in adults. It has been reported that mitochondrial dysfunction in chondrocytes was associated with osteoarthritis. Puerarin has multiple effects including restoring mitochondrial function. In this study, the potential effects of puerarin on osteoarthritis and osteoarthritis associated mitochondrial dysfunctions were evaluated. Methods: Osteoarthritis rats were treated with puerarin and the severity of osteoarthritis and cartilage damages was evaluated. The mitochondrial biogenesis and functions were analyzed by measuring related proteins expression, mitochondrial DNA content, ATP production, and oxygen consumption. The dependence of AMP-activated protein kinase (AMPK) pathway on puerarin-regulated mitochondrial function was analyzed by applying AMPK inhibitor Compound C. Results: Puerarin treatment alleviated mechanical hyperalgesia and cartilage damage in osteoarthritis rats. Puerarin increased mitochondrial biogenesis and attenuated mitochondrial dysfunctions in osteoarthritis rats. AMPK inhibitor Compound C abolished puerarin’s effects. Conclusion: Puerarin attenuates osteoarthritis by upregulating the AMPK/proliferator-activated receptor-γ coactivator signaling pathway in osteoarthritis rats.

scholarly journals Blockade of TRPM7 Alleviates Chondrocyte Apoptosis and Articular Cartilage Damage in the Adjuvant Arthritis Rat Model Through Regulation of the Indian Hedgehog Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Ganggang Ma ◽  
Yang Yang ◽  
Yong Chen ◽  
Xin Wei ◽  
Jie Ding ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Signaling Pathway ◽  
Rat Model ◽  
Adjuvant Arthritis ◽  
Hedgehog Signaling ◽  
Cartilage Damage ◽  
Chondrocyte Apoptosis ◽  
Indian Hedgehog ◽  
Hedgehog Signaling Pathway ◽  
Articular Cartilage Damage

Articular cartilage damage with subsequent impairment of joint function is a common feature of articular diseases, in particular, rheumatoid arthritis and osteoarthritis. While articular cartilage injury mediated by chondrocyte apoptosis is a known major pathological feature of arthritis, the specific mechanisms remain unclear at present. Transient receptor potential melastatin-like seven channel (TRPM7) is reported to play an important regulatory role in apoptosis. This study focused on the effects of TRPM7 on arthritic chondrocyte injury and its underlying mechanisms of action. Sodium nitroprusside (SNP)-induced rat primary chondrocyte apoptosis and rat adjuvant arthritis (AA) were used as in vitro and in vivo models, respectively. Blockage of TRPM7 with 2-APB or specific siRNA resulted in increased chondrocyte viability and reduced toxicity of SNP. Moreover, treatment with 2-APB enhanced the Bcl-2/Bax ratio and reduced cleaved PARP and IL-6, MMP-13 and ADAMTS-5 expression in SNP-treated chondrocytes. Activation of Indian Hedgehog with purmorphamine reversed the protective effects of 2-APB on SNP-induced chondrocyte apoptosis. Blockage of TRPM7 with 2-APB relieved the clinical signs of AA in the rat model and reduced the arthritis score and paw swelling. Similar to findings in SNP-treated chondrocytes, 2-APB treatment increased the Bcl-2/Bax ratio and suppressed cleaved PARP, IL-6, MMP-13, ADAMTS-5, TRPM7, and Indian hedgehog expression in articular cartilage of AA rats. Our collective findings suggest that blockade of TRPM7 could effectively reduce chondrocyte apoptosis and articular cartilage damage in rats with adjuvant arthritis through regulation of the Indian Hedgehog signaling pathway.

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