Paeoniflorin suppresses IL-6/Stat3 pathway via upregulation of Socs3 in dendritic cells in response to 1-chloro-2,4-dinitrobenze

Shi, Dongmei; Wang, Qiong; Zheng, Hailin; Li, Dongmei; Shen, Ya; Fu, Hongjun; Li, Tianhang; Mei, Huan; Lu, Guangming; Qiu, Ying; Liu, Weida

doi:10.1016/j.intimp.2016.05.013

Cited by 13 publications

(7 citation statements)

References 33 publications

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“…These results indicate that induction of IL-6, TNF-α and MIP-2 by LPS may not be directly affected by the STAT3 transcription factor in the nucleus. Alternatively, the binding of IL-6 to its receptor may induce phosphorylation of JAK/STAT and its subsequent translocation to the nucleus (37,38).…”

Section: Discussionmentioning

confidence: 99%

Chlorogenic acid suppresses lipopolysaccharide-induced nitric oxide and interleukin-1β expression by inhibiting JAK2/STAT3 activation in RAW264.7 cells

Kim

Park

et al. 2017

Molecular Medicine Reports

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Chlorogenic acid (CA) is a phenolic compound purified from coffee, fruits and their associated beverages, which possess various biological properties, such as antioxidant and anticarcinogenic activities. The present study evaluated the effects of CA on lipopolysaccharide (LPS)‑induced inflammation in RAW264.7 cells and the associated intracellular signaling pathways using reverse transcription‑quantitative polymerase chain reaction, western blotting and enzyme‑linked immunosorbent assays. CA pretreatment inhibited LPS‑induced expression of inducible nitric oxide synthase (iNOS), nitric oxide (NO) and pro‑inflammatory mediators including interleukin (IL)‑6, tumor necrosis factor‑α (TNF‑α), macrophage inflammatory protein‑2 (MIP‑2) and IL‑1β in RAW264.7 cells. In addition, phosphorylation of Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) with LPS was inhibited by CA pretreatment. CA and STAT3 inhibitor (STAT3i) pretreatment inhibited LPS‑induced nuclear translocation of phosphorylated STAT3. In addition, STAT3i inhibited the LPS‑induced expression of iNOS, NO and IL‑1β similar to the results of CA pretreatment. By contrast, STAT3i did not inhibit the LPS‑induced increase in IL‑6, TNF‑α and MIP‑2 expression. These results indicate that CA may suppress LPS‑induced NO and IL‑1β expression by inhibiting JAK2/STAT3 activation in RAW264.7 cells.

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Section: Discussionmentioning

confidence: 99%

Chlorogenic acid suppresses lipopolysaccharide-induced nitric oxide and interleukin-1β expression by inhibiting JAK2/STAT3 activation in RAW264.7 cells

Kim

Park

et al. 2017

Molecular Medicine Reports

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“…Previous studies have reported that PF exerts anti-inflammatory effects in order to regulate cellular functions (27)(28)(29)(30).…”

Section: Discussionmentioning

confidence: 99%

Paeoniflorin protects PC12 cells from oxygen-glucose deprivation/reoxygenation-induced injury via activating JAK2/STAT3 signaling

Zhang

Yang

2021

Exp Ther Med

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Ischemic stroke is the most common type of stroke, and it has become a major health issue as it is characterized by high mortality and morbidity rates. Paeoniflorin (PF) is a natural compound and the main active ingredient of Radix Paeoniae. The aim of the present study was to investigate the role of PF in oxygen-glucose deprivation/reoxygenation (OGD/R)-induced injury of PC12 cells and its association with the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. An in vitro model of OGD/R injury was established in PC12 cells. Subsequently, Cell Counting Kit-8 assay and ELISA were used to evaluate cell viability and the secretion of inflammatory factors, respectively, in PC12 cells subjected to OGD/R and treated with PF. The levels of oxidative stress indicators and inflammatory factors were measured using corresponding commercial kits. In addition, the apoptosis rate of PC12 cells subjected to OGD/R and treated with PF was determined by flow cytometry, and the expression of apoptosis-related proteins was analyzed by western blotting. Additionally, the expression levels of JAK2/STAT3 pathway-related proteins were also evaluated. The cell viability, levels of oxidative stress, inflammation and apoptosis were also measured in OGD/R-induced PC12 cell injury models following co-treatment of cells with PF and FLLL32, a specific inhibitor of JAK2/STAT3 signaling. Cell viability was reduced, while oxidative stress and inflammation were increased after OGD/R-induced injury. However, the treatment of cells with PF significantly enhanced cell viability, and alleviated oxidative stress, inflammation and apoptosis of OGD/R-treated PC12 cells. Furthermore, PF activated the JAK2/STAT3 signaling pathway. Following FLLL32 intervention, the effects of PF on oxidative stress, inflammation and apoptosis of OGD/R-treated PC12 cells were reversed. In conclusion, the findings of the present study suggested that PF may protect PC12 cells from OGD/R-induced injury via activating the JAK2/STAT3 signaling pathway, thus providing novel insight into the mechanism through which PF may alleviate ischemic stroke and indicating a potential strategy for ischemic stroke treatment.

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“…Certain components of KJL may contribute to the effect on the STAT3 signaling pathway. Paeoniflorin, a main active ingredient in Paeonia, suppresses STAT3 phosphorylation and promotes STAT3 degradation [40, 41]. Atractylenolide II in Atractylodes has exhibited inhibitory effects on STAT3 phosphorylation in other cells [42].…”

Section: Discussionmentioning

confidence: 99%

Kuijieling-Containing Serum Regulates Th17 and Treg Cell Differentiation by Inhibiting STAT3 Signaling In Vitro

Jie

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Object. To investigate the effect of Kuijieling (KJL) on the balance between T helper 17 (Th17) and regulatory T (Treg) cells in peripheral blood mononuclear cells (PBMC) in vitro and explore the underlying mechanism. Materials and Methods. PBMCs isolated from rats were stimulated with transforming growth factor-β, interleukin (IL)-6, and IL-23 to induce the imbalance of Th17 and Treg cells and were treated with 10, 5, or 2.5% KJL-containing serum. The proportion of Th17 or Treg cells in CD4+ T cells was analyzed by flow cytometry, the concentrations of IL-17, IL-21, and IL-10 were assayed by ELISA, mRNA expressions of retinoic acid-related orphan receptor γt (RORγt), forkhead box protein 3 (Foxp3), and signal transducer and activator of transcription 3 (STAT3) were quantified by PCR, and phosphorylated STAT3 (p-STAT3) was analyzed by flow cytometry. Results. KJL-containing serum decreased the proportion of Th17 cells and increased the proportion of Treg cells in CD4+ T cells, decreased the concentration of IL-17 and IL-21, enhanced the level of IL-10 in the cell culture supernatant, promoted the expression of Foxp3, and inhibited the levels of RORγt, STAT3, and p-STAT3. Conclusion. KJL suppresses the STAT3 pathway to remedy the imbalance between Th17 and Treg cells.

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Paeoniflorin suppresses IL-6/Stat3 pathway via upregulation of Socs3 in dendritic cells in response to 1-chloro-2,4-dinitrobenze

Cited by 13 publications

References 33 publications

Chlorogenic acid suppresses lipopolysaccharide-induced nitric oxide and interleukin-1β expression by inhibiting JAK2/STAT3 activation in RAW264.7 cells

Chlorogenic acid suppresses lipopolysaccharide-induced nitric oxide and interleukin-1β expression by inhibiting JAK2/STAT3 activation in RAW264.7 cells

Paeoniflorin protects PC12 cells from oxygen-glucose deprivation/reoxygenation-induced injury via activating JAK2/STAT3 signaling

Kuijieling-Containing Serum Regulates Th17 and Treg Cell Differentiation by Inhibiting STAT3 Signaling In Vitro

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