Blocking Smad2 signalling with loganin attenuates SW10 cell cycle arrest induced by TNF-α

Gao, Chao; Tian, Xiaoning; Zhang, Wentao; Ou, Xuehai; Fang, Cong; Song, Tao

doi:10.1371/journal.pone.0176965

Cited by 16 publications

(15 citation statements)

References 31 publications

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“…Wang et al verified that loganin alleviates intestinal epithelial inflammation by regulating the TLR4/NF-κB and JAK/STAT3 signaling pathways [ 41 ]. Chao et al exhibited that loganin has beneficial effects on Schwann cells by blocking Smad2 signaling induced by TNF-α [ 42 ]. Chen et al found that loganin can reduce ROS and suppress the RAGE/p38 MAPK/NF-κB pathway to alleviate germ cell apoptosis in diabetes mellitus [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Loganin Attenuates High Glucose-Induced Schwann Cells Pyroptosis by Inhibiting ROS Generation and NLRP3 Inflammasome Activation

Cheng

Chu²,

Chen

et al. 2020

Cells

117

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Diabetic peripheral neuropathy (DPN) is caused by hyperglycemia, which induces oxidative stress and inflammatory responses that damage nerve tissue. Excessive generation of reactive oxygen species (ROS) and NOD-like receptor protein 3 (NLRP3) inflammasome activation trigger the inflammation and pyroptosis in diabetes. Schwann cell dysfunction further promotes DPN progression. Loganin has been shown to have antioxidant and anti-inflammatory neuroprotective activities. This study evaluated the neuroprotective effect of loganin on high-glucose (25 mM)-induced rat Schwann cell line RSC96 injury, a recognized in vitro cell model of DPN. RSC96 cells were pretreated with loganin (0.1, 1, 10, 25, 50 μM) before exposure to high glucose. Loganin’s effects were examined by CCK-8 assay, ROS assay, cell death assay, immunofluorescence staining, quantitative RT–PCR and western blot. High-glucose-treated RSC96 cells sustained cell viability loss, ROS generation, NF-κB nuclear translocation, P2 × 7 purinergic receptor and TXNIP (thioredoxin-interacting protein) expression, NLRP3 inflammasome (NLRP3, ASC, caspase-1) activation, IL-1β and IL-18 maturation and gasdermin D cleavage. Those effects were reduced by loganin pretreatment. In conclusion, we found that loganin’s antioxidant effects prevent RSC96 Schwann cell pyroptosis by inhibiting ROS generation and suppressing NLRP3 inflammasome activation.

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Section: Discussionmentioning

confidence: 99%

Loganin Attenuates High Glucose-Induced Schwann Cells Pyroptosis by Inhibiting ROS Generation and NLRP3 Inflammasome Activation

Cheng

Chu²,

Chen

et al. 2020

Cells

117

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“…In addition, the BL2 subtype does not respond to any classical treatment [48]. Taking these observations into consideration, the cytokines as well as calcitriol and its analogue could be inhibiting proliferation in SUM-229PE cells by inducing cell cycle arrest, as it has been observed in other tissues [49–52]. This requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

Calcitriol Inhibits the Proliferation of Triple-Negative Breast Cancer Cells through a Mechanism Involving the Proinflammatory Cytokines IL-1βand TNF-α

Martínez-Reza

Díaz

Barrera

et al. 2019

Journal of Immunology Research

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Triple-negative breast cancer (TNBC) is one of the most aggressive tumors, with poor prognosis and high metastatic capacity. The aggressive behavior may involve inflammatory processes characterized by deregulation of molecules related to the immunological responses in which interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α) are involved. It is known that calcitriol, the active vitamin D metabolite, modulates the synthesis of immunological mediators; however, its role in the regulation of IL-1βand TNF-αin TNBC has been scarcely studied. In the present study, we showed that TNBC cell lines SUM-229PE and HCC1806 expressed vitamin D, IL-1β, and TNF-αreceptors. Moreover, calcitriol, its analogue EB1089, IL-1β, and TNF-αinhibited cell proliferation. In addition, we showed that synthesis of both IL-1βand TNF-αwas stimulated by calcitriol and its analogue. Interestingly, the antiproliferative activity of calcitriol was significantly abrogated when the cells were treated with anti-IL-1βreceptor 1 (IL-1R1) and anti-TNF-αreceptor type 1 (TNFR1) antibodies. Furthermore, the combination of calcitriol with TNF-αresulted in a greater antiproliferative effect than either agent alone, in the two TNBC cell lines and an estrogen receptor-positive cell line. In summary, this study demonstrated that calcitriol exerted its antiproliferative effects in part by inducing the synthesis of IL-1βand TNF-αthrough IL-1R1 and TNFR1, respectively, in TNBC cells, highlighting immunomodulatory and antiproliferative functions of calcitriol in TNBC tumors.

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“…In addition, Loganin exhibits neuroprotection (Kwon et al, ), anti‐amnesic activity (Lee et al, ), protective effects against neurodegenerative diseases (Kwon, Kim, Lee, & Jang, ), hepatic injury, and other diabetic complications (Yamabe et al, ). In Schwann SW10 cells, Loganin blocks the effects of TNF‐α (Chao et al, ). Loganetin is produced by the deglucosylation of Loganin (Miettinen et al, ).…”

Section: Discussionmentioning

confidence: 99%

Loganetin protects against rhabdomyolysis‐induced acute kidney injury by modulating the toll‐like receptor 4 signalling pathway

Tan

Wang

et al. 2019

British J Pharmacology

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Background and Purpose: Acute kidney injury (AKI) is a rapid renal dysfunctional disease, for which no effective drugs or therapies are available to improve prognosis.Loganetin is a natural product with unknown bioactivities. Here, we identified a new protective effect and mechanism of Loganetin in a mouse model of AKI induced by rhabdomyolysis.Experimental Approach: AKI was induced using glycerol by i.m. injection in mice models. Thirty minutes and 24 and 48 hr after injection of glycerol, the mice received 2 and 18 mg·kg −1 of Loganetin i.p. respectively. Then mice blood and kidney were collected for various biochemical and histopathological studies. Mechanistic studies on modulation of AKI by Loganetin were performed using HK-2 cells and Toll-like receptor 4 (TLR4) knockout mice.Key Results: In the Loganetin treated group, kidney damage and mortality rate were declined, and blood urea nitrogen and serum creatinine were much lower. Loganetin prevented damage to the tubular structures induced by glycerol and decreased apoptotic cells at the corticomedullary junction. In HK-2 cells, Loganetin could inhibit NF-κB pathway and pro-apoptotic genes expression. However, TLR4 was silenced by a specific shRNA, and the inhibitory effect of Loganetin in HK-2 cells vanished. Loganetin also down-regulated the expression of inflammation factors by suppressing TLR4 activity.Conclusion and Implications: All the results suggested that TLR4 plays a critical role in AKI development, and Loganetin ameliorates AKI by inhibiting TLR4 activity and blocking the JNK/p38 pathway, which provides a new strategy for AKI treatment.

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Blocking Smad2 signalling with loganin attenuates SW10 cell cycle arrest induced by TNF-α

Cited by 16 publications

References 31 publications

Loganin Attenuates High Glucose-Induced Schwann Cells Pyroptosis by Inhibiting ROS Generation and NLRP3 Inflammasome Activation

Loganin Attenuates High Glucose-Induced Schwann Cells Pyroptosis by Inhibiting ROS Generation and NLRP3 Inflammasome Activation

Calcitriol Inhibits the Proliferation of Triple-Negative Breast Cancer Cells through a Mechanism Involving the Proinflammatory Cytokines IL-1βand TNF-α

Loganetin protects against rhabdomyolysis‐induced acute kidney injury by modulating the toll‐like receptor 4 signalling pathway

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