Triptolide suppresses airway goblet cell hyperplasia and Muc5ac expression via NF-κB in a murine model of asthma

Chen, Ming; Lv, Zhiqiang; Zhang, Wei; Huang, Lixiang; Lin, Xiaoling; Shi, Jianting; Zhang, Wei; Liang, Ruiyun; Jiang, Shanping

doi:10.1016/j.molimm.2014.11.001

Cited by 27 publications

(20 citation statements)

References 24 publications

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“…In total, 6 rats were included in the sham group and 30 rats were included in the I/R group for the present study. In the I/R group, rats were further divided into subgroups with 6 rats in each subgroup according to the different reperfusion times (6,12,24, 48 and 72 h). All of the rats that survived the surgical procedures underwent subsequent neurological evaluation, and pathological and molecular experiments.…”

Section: Resultsmentioning

confidence: 99%

“…T-helper 2 (Th2) cell-associated cytokines, particularly interleukin-13 (IL-13), are thought to be key regulators of mucus production in the airway (11). In addition, classical inflammatory signaling via the nuclear factor-κB (NF-κB) signaling pathway, has also been indicated to be involved in the regulation of mucus overproduction during pathological airway remodeling (12,13). Increased levels of cytokines, such as IL-13 and other factors, trigger the activation of the NF-κB pathway in pulmonary tissues, which functions as a transcriptional factor with the nuclear translocation of its key component p65.…”

Section: Cerebral Ischemia/reperfusion Injury Induces Airway Mucus Hymentioning

confidence: 99%

“…Cerebral I/R injury-activated NF-κB inflammatory signaling pathway in lungs. As NF-κB inflammatory signaling has been implicated in the regulation of airway mucus hypersecretion (12,13), we hypothesized that cerebral I/R injury may lead to the overproduction of mucus via activation of the pulmonary NF-κB pathway. Western blot analysis revealed that cerebral I/R injury was associated with decreased protein levels of IkBs and cytoplasmic NF-κB p65, as well as increased levels of nuclear NF-κB p65 (Fig.…”

Section: Cerebral I/r Injury-activated Inflammatory Factors In Serum mentioning

confidence: 99%

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Cerebral ischemia/reperfusion injury induces airway mucus hypersecretion in rats and activates IL-13-associated inflammatory mechanisms

Zhang

Che

et al. 2017

Molecular Medicine Reports

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The majority of patients that suffer a stroke have excessive sputum, which accelerates the development of pulmonary complications. However, it is unclear whether cerebral ischemia and reperfusion (I/R) injury induces mucus hypersecretion, and the potential role of inflammation remains unknown. In the present study, the reversible middle cerebral artery occlusion model was applied in rats to induce cerebral I/R injury. The rats were grouped according to the duration of reperfusion (6, 12, 24, 48 and 72 h). Neurological dysfunction was evaluated by Longa scoring and lung dry‑to‑wet weight (dw/ww) ratios were determined to reflect the degree of mucus secretion. Inflammatory factor interleukin‑13 (IL‑13) and tumor necrosis factor‑α (TNF‑α) levels in serum and bronchoalveolar lavage fluid (BALF) were determined by enzyme‑linked immunosorbent assay. Pulmonary levels of mucin 5AC (MUC5AC) and key molecules involved in nuclear factor‑κB (NF‑κB) signaling were determined by western blotting and immunohistochemistry. Rats with cerebral I/R had impaired neurological function, which was associated with the length of reperfusion time. In addition, the dw/ww lung ratio decreased and the pulmonary expression of MUC5AC increased with the increase in severity of neurological dysfunction, indicating that cerebral I/R may induce mucus hypersecretion in a reperfusion time‑dependent manner. IL‑13 and TNF‑α levels in serum and BALF, as well as the nuclear translocation of NF‑κB p65 in pulmonary tissues, significantly increased following cerebral I/R, which suggests that the activation of IL‑13 and NF‑κB inflammatory pathways may be involved. The present study concluded that cerebral I/R injury may induce airway mucus hypersecretion by activating IL‑13 and NF‑κB inflammatory pathways.

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Section: Resultsmentioning

confidence: 99%

Section: Cerebral Ischemia/reperfusion Injury Induces Airway Mucus Hymentioning

confidence: 99%

Section: Cerebral I/r Injury-activated Inflammatory Factors In Serum mentioning

confidence: 99%

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Cerebral ischemia/reperfusion injury induces airway mucus hypersecretion in rats and activates IL-13-associated inflammatory mechanisms

Zhang

Che

et al. 2017

Molecular Medicine Reports

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“…Triptolide treatment has been shown to inhibit lung inflammation and injury in multiple lung disease models, including lipopolysaccharide injury (Wei and Huang, 2014), pulmonary fibrosis induced by radiation (Yang et al, 2015) or bleomycin (Krishna et al, 2001), and allergic inflammation and airway remodeling (Chen et al, 2011; Chen et al, 2015). In the present study, three of the triptolide formulations that were tested in vivo produced significant inhibition of chlorine-induced inflammation.…”

Section: Discussionmentioning

confidence: 99%

Development and assessment of countermeasure formulations for treatment of lung injury induced by chlorine inhalation

Hoyle

Jing

Schlueter

et al. 2016

Toxicology and Applied Pharmacology

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Chlorine is a commonly used, reactive compound to which humans can be exposed via accidental or intentional release resulting in acute lung injury. Formulations of rolipram (a phosphodiesterase inhibitor), triptolide (a natural plant product with anti-inflammatory properties), and budesonide (a corticosteroid), either neat or in conjunction with poly(lactic:glycolic acid) (PLGA), were developed for treatment of chlorine-induced acute lung injury by intramuscular injection. Formulations were produced by spray-drying, which generated generally spherical microparticles that were suitable for intramuscular injection. Multiple parameters were varied to produce formulations with a wide range of in vitro release kinetics. Testing of selected formulations in chlorine-exposed mice demonstrated efficacy against key aspects of acute lung injury. The results show the feasibility of developing microencapsulated formulations that could be used to treat chlorine-induced acute lung injury by intramuscular injection, which represents a preferred route of administration in a mass casualty situation.

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“…Triptolide has been shown to possess potent anti-inflammatory and antioxidative effects in many diseases. [14][15][16][17] Triptolide has been reported to reduce proteinuria in animal models of glomerular disease. 5 [TGFb] activated kinase 1, also known as MAP3K7 binding protein 1) as the binding target of triptolide in macrophages.…”

Section: Anti-inflammatory and Antioxidative Effects Of Traditional Mmentioning

confidence: 99%

Recent Advances in Traditional Chinese Medicine for Kidney Disease

Zhong

Menon

Deng

et al. 2015

American Journal of Kidney Diseases

109

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Triptolide suppresses airway goblet cell hyperplasia and Muc5ac expression via NF-κB in a murine model of asthma

Cited by 27 publications

References 24 publications

Cerebral ischemia/reperfusion injury induces airway mucus hypersecretion in rats and activates IL-13-associated inflammatory mechanisms

Cerebral ischemia/reperfusion injury induces airway mucus hypersecretion in rats and activates IL-13-associated inflammatory mechanisms

Development and assessment of countermeasure formulations for treatment of lung injury induced by chlorine inhalation

Recent Advances in Traditional Chinese Medicine for Kidney Disease

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