Paeoniflorin protects against lipopolysaccharide-induced acute lung injury in mice by alleviating inflammatory cell infiltration and microvascular permeability

Zhou, Haiqiang; Bian, Difei; Jiao, Xue; Wei, Zhifeng; Zhang, Haofang; Xia, Yufeng; He, Yisheng; Dai, Yue

doi:10.1007/s00011-011-0359-9

Cited by 54 publications

(28 citation statements)

References 47 publications

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“…For example, paeoniflorin suppresses the inflammatory mediators IL-1, TNF-␣, and PGE2 in type II collagen induced arthritic rats (40). Zhou et al (43) have showed that paeoniflorin protects against LPS-induced acute lung injury through downregulation of the activation of p38, JNK, and NF-B pathways. Chen et al (2) showed that paeoniflorin suppresses TNF-␣ induced chemokine production in human dermal microvascular endothelial cells, which is relevant to NF-B and ERK pathways suppression.…”

Section: Discussionmentioning

confidence: 99%

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Paeoniflorin abrogates DSS-induced colitis via a TLR4-dependent pathway

Zhang

Dou

Zhang

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

112

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Paeonia lactiflora Pall is one of the most well-known herbs in China, Korea, and Japan for more than 1,200 years. Paeoniflorin, the major bioactive component of peony root, has recently been reported to have anticolitic activity. However, the underlying molecular mechanism is unclear. The present study was to explore the possible mechanism of paeoniflorin in attenuating dextran sulfate sodium (DSS)-induced colitis. Pre- and coadministration of paeoniflorin significantly reduced the severity of colitis and resulted in downregulation of several inflammatory parameters in the colon, including the activity of myeloperoxidase (MPO), the levels of TNF-α and IL-6, and the mRNA expression of proinflammatory mediators (MCP-1, Cox2, IFN-γ, TNF-α, IL-6, and IL-17). The decline in the activation of NF-κB p65, ERK, JNK, and p38 MAPK correlated with a decrease in mucosal Toll-like receptor 4 (TLR4) but not TLR2 or TLR5 expression. In accordance with the in vivo results, paeoniflorin downregulated TLR4 expression, blocked nuclear translocation of NF-κB p65, and reduced the production of IL-6 in LPS-stimulated mouse macrophage RAW264.7 cells. Transient transfection assay performed in LPS-stimulated human colon cancer HT-29 cells indicated that paeoniflorin inhibits NF-κB transcriptional activity in a dose-dependent manner. TLR4 knockdown and overexpression experiments demonstrated a requirement for TLR4 in paeoniflorin-mediated downregulation of inflammatory cytokines. Thus, for the first time, the present study indicates that paeoniflorin abrogates DSS-induced colitis via decreasing the expression of TLR4 and suppressing the activation of NF-κB and MAPK pathways.

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Section: Discussionmentioning

confidence: 99%

“…no. 12-1001, HPLC Ն 98%) was obtained from Shanghai R&D Center for Standardization of Traditional Chinese Medicine, Shanghai, China, and the dosage selection (50 mg/kg) was based on previous in vivo studies and was confirmed to result in effective alleviation of acute lung injury and arthritis in mouse disease models (40,43).…”

Section: Methodsmentioning

confidence: 99%

Paeoniflorin abrogates DSS-induced colitis via a TLR4-dependent pathway

Zhang

Dou

Zhang

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

112

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“…In fact, in a bleomycin-induced lung fibrosis mouse model, approximately one-third of the fibroblasts in lung tissues were derived from type II lung epithelial cells that underwent EMT [9] . Paeoniflorin ( Figure 1), a pinane monoterpene glucoside found in the root of Paeonia lactiflora Pall, has been reported to have anti-inflammatory and immunomodulatory properties [10][11][12] . Recently, we demonstrated that paeoniflorin substantially prevented pulmonary fibrosis (PF) in bleomycin-treated mice by suppressing the synthesis of type I collagen in lung tissues [13] .…”

Section: Introductionmentioning

confidence: 99%

Paeoniflorin suppresses TGF-β mediated epithelial-mesenchymal transition in pulmonary fibrosis through a Smad-dependent pathway

et al. 2016

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Aim: Paeoniflorin has shown to attenuate bleomycin-induced pulmonary fibrosis (PF) in mice. Because the epithelial-mesenchymal transition (EMT) in type 2 lung endothelial cells contributes to excessive fibroblasts and myofibroblasts during multiple fibrosis of tissues, we investigated the effects of paeoniflorin on TGF-β mediated pulmonary EMT in bleomycin-induced PF mice. Methods: PF was induced in mice by intratracheal instillation of bleomycin (5 mg/kg). The mice were orally treated with paeoniflorin or prednisone for 21 d. After the mice were sacrificed, lung tissues were collected for analysis. An in vitro EMT model was established in alveolar epithelial cells (A549 cells) incubated with TGF-β1 (2 ng/mL). EMT identification and the expression of related proteins were performed using immunohistochemistry, transwell assay, ELISA, Western blot and RT-qPCR. Results: In PF mice, paeoniflorin (50, 100 mg·kg -1 ·d -1 ) or prednisone (6 mg·kg -1 ·d -1 ) significantly decreased the expression of FSP-1 and α-SMA, and increased the expression of E-cadherin in lung tissues. In A549 cells, TGF-β1 stimulation induced EMT, as shown by the changes in cell morphology, the increased cell migration, and the increased vimentin and α-SMA expression as well as type I and type III collagen levels, and by the decreased E-cadherin expression. In contrast, effects of paeoniflorin on EMT disappeared when the A549 cells were pretreated with TGF-β1 for 24 h. TGF-β1 stimulation markedly increased the expression of Snail and activated Smad2/3, Akt, ERK, JNK and p38 MAPK in A549 cells. Co-incubation with paeoniflorin (1-30 µmol/L) dose-dependently attenuated TGF-β1-induced expression of Snail and activation of Smad2/3, but slightly affected TGF-β1-induced activation of Akt, ERK, JNK and p38 MAPK. Moreover, paeoniflorin markedly increased Smad7 level, and decreased ALK5 level in A549 cells. Conclusion: Paeoniflorin suppresses the early stages of TGF-β mediated EMT in alveolar epithelial cells, likely by decreasing the expression of the transcription factors Snail via a Smad-dependent pathway involving the up-regulation of Smad7.

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“…Similar effects of paeoniflorin on the severity of hind paw swelling and the scores of polyarthritis were also confirmed in the rats with experimental arthritis [19][20][21]. In addition, intraperitoneal injection of paeoniflorin inhibited the severity of intratracheal instillation of lipopolysaccharide (LPS)-induced acute lung injury in mice by suppressing inflammatory cell infiltration and lowing microvascular permeability [22]. Subcutaneous injection of TGP also inhibited capillary permeability associated with inflammation induced by intraperitoneal injection of acetic acid in mice [23].…”

Section: Anti-inflammatory Effectsmentioning

confidence: 61%

Mechanisms involved in the therapeutic effects of Paeonia lactiflora Pallas in rheumatoid arthritis

Zhang

Dai

2012

International Immunopharmacology

131

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Paeoniflorin protects against lipopolysaccharide-induced acute lung injury in mice by alleviating inflammatory cell infiltration and microvascular permeability

Abstract: The findings suggest that PF is able to alleviate ALI, and the underlying mechanisms are probably attributed to decreasing the production of proinflammatory cytokines through down-regulation of the activation of p38, JNK and NF-κB pathways in lung tissues.

Cited by 54 publications

References 47 publications

Paeoniflorin abrogates DSS-induced colitis via a TLR4-dependent pathway

Paeoniflorin abrogates DSS-induced colitis via a TLR4-dependent pathway

Paeoniflorin suppresses TGF-β mediated epithelial-mesenchymal transition in pulmonary fibrosis through a Smad-dependent pathway

Mechanisms involved in the therapeutic effects of Paeonia lactiflora Pallas in rheumatoid arthritis

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