Loganin ameliorates cartilage degeneration and osteoarthritis development in an osteoarthritis mouse model through inhibition of NF-κB activity and pyroptosis in chondrocytes

Hu, Jiaming; Zhou, Jinyi; Wu, Jinting; Chen, Quan; Du, Weibin; Fu, Fangda; Yu, Huan; Yao, Sai; Jin, Hongting; Tong, Peijian; Chen, Di; Wu, Chengliang; Ruan, Hongfeng

doi:10.1016/j.jep.2019.112261

Cited by 106 publications

(96 citation statements)

References 32 publications

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“…After then, the active Caspase-1 was released from it and further to hydrolyzes pro-IL-1β into mature IL-1β [34]. Our previous finding was consistent with those of the latter study, which demonstrated Nlrp3 inflammasome-mediated pyroptosis was induced during the progression of OA [33,34]. However, the role of pyroptosis during the progression of IVDD and WBV is not yet utterly understood.…”

Section: Wbv Activates Wnt/β-catenin Signaling Pathway Of Ivdd Micesupporting

confidence: 90%

“…Studies have found that a cause of discogenic LBP is IVD inflammation and axonal growth of afferent fibers innervating the disc, and IL-1β is a pain-related molecule that was significantly elevated in painful human IVD [32]. We have previously reported that Nlrp3 inflammasome-mediated pyroptosis is proinflammatory and produces an excessive level of cartilage-degrading cytokines, including IL-1β [33]. To date, the relationship between pyroptosis and IVDD is still obscure.…”

Section: Wbv Attenuates Caspase-1 and Il-1β Expression In Ivdd Micementioning

confidence: 99%

“…Persistent inflammation in painful discs, and that the production of these molecules may be a major factor in discogenic LBP. Nlrp3-mediated pyroptosis is a new form of programmed inflammatory cell death that participates in the inflammatory response by releasing a plentiful of cartilage-degrading cytokines, including IL-1β [33]. After Nlrp3 binds its adaptor apoptosis-associated speck-like protein, pro-Caspase-1 will be recruited to assemble Nlrp3 inflammasome.…”

Section: Wbv Activates Wnt/β-catenin Signaling Pathway Of Ivdd Micementioning

confidence: 99%

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Whole-body Vibration Attenuates Pyroptosis-Mediated Inflammation but Accelerates Progression of Intervertebral Disc Degeneration

Yao

Sun³

et al. 2020

Preprint

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Background Whole body vibration (WBV) is a non-pharmaceutical therapy that has been widely incorporated into clinical practice for musculoskeletal disorders, including low back pain (LBP). Intervertebral disc (IVD) degeneration (IVDD) is clinically associated with LBP and is known as the main cause for LBP. However, cumulative evidence also suggested WBV might have an adverse impact on IVDs. Moreover, previous studies have been focusing on the effects of WBV on healthy mice, rather than those suffering from IVDD. Thus, uncertainties still exist concerning the effects of WBV on IVDs undergoing IVDD. This study was aiming to evaluate the effects of WBV intervention on the development and progression of IVDD mouse model induced by lumbar spine instability (LSI) surgery. Methods LSI surgery, by resecting the lumbar 3 rd -5 th spinous processes along with the supraspinous and interspinous ligaments, was conducted in 10-week-old male mice which then received WBV treatment (1 h per day, 5 days per week, at 3 Hz with peak acceleration at 0.4 g) or sham treatment. The progression of IVDD was evaluated by MRI, μCT and histological analyses after WBV treatment. The matrix metabolism, distribution of sensory nerves, pyroptosis in IVDs tissues were determined by immunohistological analysis or real-time PCR. The apoptosis of IVD cells was detected by TUNEL assay. Results LSI surgery was successful in producing IVDD modeling. WBV caused decreases in IVD height and annulus fibrosus (AF) score, as well as increased numbers of apoptotic cells in IVD tissues. WBV contributed to sensory innervation into AF and upregulation of Adamts5 and MMP3 expression in IVDD mice received LSI surgery. In addition, WBV treatment triggered earlier activation of Wnt/β-catenin signaling in IVDD mice with WBV treatment compared with those without WBV treatment. Unexpectedly, WBV significantly attenuated Caspase-1 and IL-1β expression in AF. Conclusions Collectively, our findings demonstrate that WBV treatment may worsen the development of ongoing IVDD. Decrease of IL-1β expression after WBV intervention may partially account for patient self-reported pain relief after WBV treatment in some previous trials. This study may help us better understand the effects of WBV intervention on patients experiencing LBP resulting from the degeneration of lumbar IVDs.

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Section: Wbv Activates Wnt/β-catenin Signaling Pathway Of Ivdd Micesupporting

confidence: 90%

Section: Wbv Attenuates Caspase-1 and Il-1β Expression In Ivdd Micementioning

confidence: 99%

Section: Wbv Activates Wnt/β-catenin Signaling Pathway Of Ivdd Micementioning

confidence: 99%

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Whole-body Vibration Attenuates Pyroptosis-Mediated Inflammation but Accelerates Progression of Intervertebral Disc Degeneration

Yao

Sun³

et al. 2020

Preprint

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“…Endoplasmic reticulum-related pyroptosis plays a role in the pathogenesis of steatohepatitis. In chondrocytes, pyroptosis modulates cell viability and ECM synthesis (Hu et al, 2020). However, the role of pyroptosis in IVD degeneration is unclear.…”

Section: Introductionmentioning

confidence: 99%

miRNA-141 Induced Pyroptosis in Intervertebral Disk Degeneration by Targeting ROS Generation and Activating TXNIP/NLRP3 Signaling in Nucleus Pulpous Cells

Xing

et al. 2020

Front. Cell Dev. Biol.

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The role and mechanism of pyroptosis in intervertebral disk (IVD) degeneration are unclear. MicroRNAs (miRNAs) regulate the viability and function of nucleus pulposus cells (NPCs) in IVDs and are related to pyroptosis. We performed microarray analyses of normal and degenerated nucleus pulposus (NP) to assess the role of pyroptosis and identify key miRNAs in IVD degeneration. We also evaluated the underlying mechanism of miRNA-mediated pyroptosis in NPCs. In addition, we demonstrated the preventative effects of miRNAs on IVD degeneration in a rat model. The levels of the pyroptosis-related proteins cleaved caspase-1, N-terminal gasdermin D (GSDMD), interleukin (IL)-1β, and IL-18 in the degenerative NP were significantly higher than those in the normal NP. miRNA-141 was significantly upregulated in the degenerated NP. miR-141 mimic suppressed the matrix synthesis function of NPCs. By contrast, reactive oxygen species (ROS) generation, and the expression of TXNIP and NLRP3 were significantly downregulated by an miR-141 inhibitor. Furthermore, the miRNA-141 inhibitor prevented the degeneration of IVDs in vivo. Our findings suggest that miRNA-141 induces pyroptosis and extracellular matrix (ECM) catabolism in NPCs by increasing ROS generation and activating TXNIP/NLRP3 signaling. miRNA-141regulated pyroptosis may be a novel therapeutic target for IVD degeneration.

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“…In this investigation, only one kind of cells was used for LPS stimulation, which was relatively simple and could not fully reflect the pathophysiological characteristics of OA. Besides, the results of our research disclosed that MF was highly effective in protecting ATDC5 cells against LPS-induced inflammatory injury, while other researches about the efficacy of scutellarin and loganin were largely focused on their functions on cartilage degeneration (Hu et al, 2020;Liu et al, 2020). Therefore, further researches still need to be done using multicells, multi-stimulation and animal models to disclose the pathogenesis of OA, and identifying the most effective therapeutic strategies for the treatment of OA.…”

Section: Resultsmentioning

confidence: 84%

Mangiferin Relieves Lipopolysaccharide-Induced Injury by Up-Regulating miR-181a via Targeting PTEN in ATDC5 Cells

Liu

et al. 2020

Front. Pharmacol.

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Background: Mangiferin (MF) was reported to possess anti-inflammatory activity. This investigation tried to probe into the underlying mechanism of MF in osteoarthritis.Methods: ATDC5 cells were pretreated with series concentrations of MF (0.1, 1, 5, 10, 15, 20 mM) for 2 h and then were exposed to lipopolysaccharide (LPS) (5 mg/ml) for 12 h to construct the inflammatory injury model. The cell viability, productions of pro-inflammatory cytokines and enzymes were respectively measured by employing CCK-8 assay, western blot, ELISA, and quantitative reverse-transcription (qRT)-PCR. miR-181a expression was altered by employing cell transfection. Dichloro-dihydro-fluorescein diacetate (DCFH-DA) method was employed for detection of reactive oxygen species (ROS) generation. Dual luciferase activity assay was conducted for analyzing the relationship between miR-181a and PTEN. The underlying mechanism was determined by employing western blot.Results: High doses of MF treatment (15 and 20 mM) noticeably induced inflammatory injury exhibiting as increased the productions of pro-inflammatory cytokines, enzymes and ROS, activated NF-kB pathway and deactivated PTEN/PI3K/AKT pathway in ATDC5 cells. Besides, MF treatment notably remitted LPS-induced inflammatory injury through deactivation of NF-kB pathway and activation of PTEN/PI3K/AKT pathway. PTEN was a target of miR-181a. Inhibition of miR-181a remarkably reversed MF-triggered impacts on ATDC5 cells.Conclusion: MF attenuated LPS-induced inflammatory damage through miR-181a/ PTEN axis and thereby inhibiting NF-kB pathway and activating PI3K/AKT pathway.

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Loganin ameliorates cartilage degeneration and osteoarthritis development in an osteoarthritis mouse model through inhibition of NF-κB activity and pyroptosis in chondrocytes

Cited by 106 publications

References 32 publications

Whole-body Vibration Attenuates Pyroptosis-Mediated Inflammation but Accelerates Progression of Intervertebral Disc Degeneration

Whole-body Vibration Attenuates Pyroptosis-Mediated Inflammation but Accelerates Progression of Intervertebral Disc Degeneration

miRNA-141 Induced Pyroptosis in Intervertebral Disk Degeneration by Targeting ROS Generation and Activating TXNIP/NLRP3 Signaling in Nucleus Pulpous Cells

Mangiferin Relieves Lipopolysaccharide-Induced Injury by Up-Regulating miR-181a via Targeting PTEN in ATDC5 Cells

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