Effects of platycodin D on IL-1ß-induced inflammatory response in human osteoarthritis chondrocytes.

Platycodin D (PYD), a major saponin derived and isolated from the roots of Platycodon grandiflorum, has been reported to have anti-inflammatory and anti-tumor effects. The present study aimed to investigate the effects of PYD on IL-1ß-stimulated human osteoarthritis chondrocytes. Chondrocytes were treated with PYD 1h before IL-1ß treatment. The levels of MMP1, MMP13, IL-8, RANTES, PGE2, and NO were measured in this study. The expression of LXRα, NF-κB, and IκBα were detected by western blot analysis. The results showed that PYD significantly inhibited IL-1ß-induced MMP1, MMP13, IL-8, RANTES, PGE2, and NO production. PYD also suppressed IL-1ß-induced NF-κB activation. Furthermore, the expression of LXRα was up-regulated by PYD in a dose-dependent manner. In addition, LXRα siRNA inhibited the effects of PYD on MMP1, MMP13, PGE2, and NO production in human osteoarthritis chondrocytes. In conclusion, these results suggested that PYD attenuated IL-1ß-induced inflammatory response in osteoarthritis chondrocyte by activating LXRα.

Platycodin D attenuates acute lung injury by suppressing apoptosis and inflammation in vivo and in vitro.

Platycodin D (PLD) is the major triterpene saponin in the root of Platycodon grandiflorum (Jacq.) with various pharmacological activities. The purpose of the present study was to evaluate the protective effects and possible mechanisms of PLD on acute lung injury (ALI) both in vivo and in vitro. In vivo, we used two ALI models, lipopolysaccharide (LPS)-induced ALI and bleomycin (BLE)-induced ALI to evaluate the protective effects and possible mechanisms of PLD. Female BALB/c mice were randomly divided into the following groups: control group, LPS group, LPS plus pre-treatment with dexamethasone (2 mg/kg) group, LPS plus pre-treatment with PLD groups (50 mg/kg, 100 mg/kg), LPS plus post-treatment with dexamethasone (2 mg/kg) group, LPS plus post-treatment with PLD groups (50 mg/kg, 100 mg/kg), BLE group, BLE plus pre-treatment with dexamethasone (2 mg/kg) group, BLE plus pre-treatment with PLD groups (50 mg/kg, 100 mg/kg), BLE plus post-treatment with dexamethasone (2 mg/kg) group, and BLE plus post-treatment with PLD groups (50 mg/kg, 100 mg/kg). PLD was orally administered before or after LPS or BLE challenge with mice. Mice were sacrificed, and lung tissues and bronchoalveolar fluid (BALF) were prepared for further analysis. Our results showed that PLD significantly decreased lung wet-to-dry weight ratio (lung W/D weight ratio), total leukocyte number and neutrophil percentage in the BALF, and myeloperoxidase (MPO) activity of lung in a dose-dependent manner. Besides, cytokine levels, including interleukin (IL)-6, tumor neurosis factor (TNF)-α were also found significantly inhibited in BALF. Furthermore, PLD effectively inhibited the expressions of nuclear factor κB (NF-κB), Caspase-3 and Bax in the lung tissues, as well as restored the expression of Bcl-2 in the lungs and improved the superoxide dismutase (SOD) activity in BALF. In vitro, we used LPS-challenged cell model to evaluate the protective effects and possible mechanisms of PLD. MLE-12 cells were stimulated with LPS in the presence and absence of PLD. The levels of TNF-α, IL-6 and the expressions of NF-κB, Caspase-3, and Bax were remarkably down-regulated, while the expression of bcl-2 was significantly up-regulated in PLD treatment groups in MLE-12 cells. These results showed that the administration of PLD improved ALI both in vivo and in vitro, possibly through suppressing apoptosis and inflammation.

Chinese bellflower root anaphylaxis: IgE-binding components and cross-reactivity with mugwort and birch.

A 56-year-old man who had suffered from seasonal rhinitis in spring and autumn experienced recurrent generalized urticaria and an oral burning sensation after eating several cooked herbs for 3 months. A skin-prick test showed positive responses to various pollens, celery, Chinese bellflower, and arrowroot. The Chinese bellflower-specific IgE ELISA OD value was 1.547. Oral challenge with unprocessed raw Chinese bellflower root provoked oral burning sensation, eyelid swelling, generalized urticaria, and hypotension. In an ELISA inhibition test, IgE binding to Chinese bellflower was significantly inhibited by Chinese bellflower, mugwort, and birch pollen extract. SDS-PAGE and immunoblot assay revealed nine IgE-binding components, and common protein bands were detected in the range of 40~55 kDa (Chinese bellflower-mugwort-birch) and 14 kDa (Chinese bellflower-birch). Chinese bellflower root can cause anaphylaxis and may have cross-reactivity with mugwort and birch.

Chinese Bellflower Root Anaphylaxis: IgE-Binding Components and Cross-Reactivity With Mugwort and Birch

A 56-year-old man who had suffered from seasonal rhinitis in spring and autumn experienced recurrent generalized urticaria and an oral burning sensation after eating several cooked herbs for 3 months. A skin-prick test showed positive responses to various pollens, celery, Chinese bellflower, and arrowroot. The Chinese bellflower-specific IgE ELISA OD value was 1.547. Oral challenge with unprocessed raw Chinese bellflower root provoked oral burning sensation, eyelid swelling, generalized urticaria, and hypotension. In an ELISA inhibition test, IgE binding to Chinese bellflower was significantly inhibited by Chinese bellflower, mugwort, and birch pollen extract. SDS-PAGE and immunoblot assay revealed nine IgE-binding components, and common protein bands were detected in the range of 40~55 kDa (Chinese bellflower-mugwort-birch) and 14 kDa (Chinese bellflower-birch). Chinese bellflower root can cause anaphylaxis and may have cross-reactivity with mugwort and birch.