Anti-Inflammatory Effects of Lagerstroemia ovalifolia Teijsm. & Binn. in TNFα/IFNγ-Stimulated Keratinocytes.

Ethnopharmacological Relevance. Atopic dermatitis is a chronic inflammatory skin disease. Lagerstroemia ovalifolia Teijsm. & Binn. (LO) has traditionally been used as an herbal medicine for anti-inflammatory diseases. The effect of LO on atopic dermatitis has not been verified scientifically. We investigated the effects of CHCl3 fraction number 5 of LO (LOC) on atopic dermatitis through cell-based experiments. HaCaT cells were treated with tumor necrosis factor-alpha (TNFα)/interferon-gamma (IFNγ) to induce an inflammatory reaction. Proinflammatory cytokines, interleukin- (IL-) 6, IL-8, and IL-1ß and chemokines such as thymus and activation-regulated chemokine (TARC/CCL17), monocyte chemoattractant protein 1 (MCP1/CCL2), and macrophage-derived chemokine (MDC/CCL22) were measured by RT-PCR and ELISA. In addition, the degree of phosphorylation and activation of JAK/STAT1, PI3K/AKT, and nuclear factor-kappa B (NF-κB) were measured by western blot and luciferase assays. The production of inflammatory cytokines and chemokines and activation of the JAK/STAT1, PI3K/AKT, and NF-κB pathways were induced by TNFα/IFNγ in HaCaT cells. Under these conditions, LOC treatment inhibited the production of targeted cytokines and chemokines and decreased the phosphorylation and activation of JAK/STAT1, PI3K/AKT, and NF-κB. These results suggest that LOC reduces the production of proinflammatory cytokines and chemokines by suppressing the JAK/STAT1, PI3K/AKT, and NF-κB pathways. Therefore, LOC may have potential as a drug for atopic dermatitis.

Physalis peruviana L. inhibits ovalbumin­induced airway inflammation by attenuating the activation of NF­κB and inflammatory molecules.

Physalis peruviana L. (PP) is well known for its various properties, including its antioxidant property. In our previous study, the protective effects of PP against cigarette smoke­induced airway inflammation were confirmed. The purpose of the present study was to evaluate the anti­inflammatory effect of PP against ovalbumin (OVA)­induced airway inflammation. Treatment with PP inhibited the numbers of eosinophils and the levels of inflammatory cytokines, including interleukin (IL)­4, IL­5 and IL­13, in the bronchoalveolar lavage fluid (BALF) of animal models with OVA­induced allergic asthma. PP also significantly decreased the production of total immunoglobulin E in the serum. Lung sections stained with hematoxylin and eosin revealed that the influx of inflammatory cells was decreased in the lungs of mice treated with PP compared with cells in the OVA group. The increased expression levels of monocyte chemoattractant protein­1 (MCP­1) and T cell marker KEN­5 were also reduced following PP treatment in the lung tissues compared with those in the OVA group. The PAS staining results showed that PP attenuated the overproduction of mucus in the lung. Additionally, western blot analysis revealed that PP significantly downregulated the activation of nuclear factor­κB/p38 mitogen­activated protein kinase/c­Jun N­terminal kinase, and upregulated the expression of heme oxgenase­1 in the lungs. In an in vitro experiment, PP effectively reduced the levels of LPS­stimulated MCP­1 in a concentration­dependent manner. Taken together, these results indicate that PP has considerable potential in the treatment of allergic asthma.

Anti-inflammatory effects of Passiflora foetida L. in LPS-stimulated RAW264.7 macrophages.

Passiflora foetida L. (Passifloraceae), a perennial climber in general, is used for treating many ailments in conventional medicine. In this study, the anti-inflammatory effect of methanolic extracts of P. foetida L. (PFME) and the involvement of nuclear factor-κB (NF-κB) signalling in the regulation of inflammation were investigated. PFME prevented the production of prostaglandin E2 (PGE2) and the expression of inducible cyclooxygenase-2 (COX-2) in lipopolysaccharide (LPS)-induced macrophage cells. Additionally, PFME reduced the release of pro-inflammatory cytokines. Moreover, in LPS-induced RAW264.7 cells, the phosphorylation of MAPKs (ERK1/2, p38 and JNK) was suppressed by PFME. Furthermore, PFME inhibited the NF-κB activation induced by LPS, which was associated with nuclear p65 levels with the abrogation of IκBα degradation and subsequent decreases. These results indicated that the PFME inhibited the LPS-induced inflammatory and oxidative responses. Therefore, we propose that the PFME may be therapeutic for treating inflammatory diseases.

Rhododendron album Blume extract inhibits TNF-α/IFN-γ-induced chemokine production via blockade of NF-κB and JAK/STAT activation in human epidermal keratinocytes.

Rhododendron album Blume (RA) has traditionally been used as an herbal medicine and is considered to have anti­inflammatory properties. It is a well­known medicine for treatment of allergic or atopic diseases. In the present study, the biological effects of an RA methanol extract (RAME) on inflammation were investigated in tumor necrosis factor­α (TNF­α)/interferon­Î³ (IFN­Î³)­stimulated human keratinocytes. The present study aimed to investigate the potential mechanisms by which RAME inhibited TNF­α/IFN­Î³­induced expression of chemokines [thymus­ and activation-regulated chemokine (TARC) and macrophage­derived chemokine (MDC)] and cytokines [interleukin (IL)­6 and IL­8] through the nuclear factor­κB (NF­κB) pathway in human keratinocytes. The effects of RAME treatment on cell viability were investigated in TNF­α/IFN­Î³­stimulated HaCaT cells. The expression of TARC, MDC, IL­6 and IL­8 was assessed using reverse transcription­quantitative polymerase chain reaction analysis or ELISA, and its effect on the inhibitory mitogen-activated protein kinase pathway was also studied using western blot analysis. TNF­α/IFN­Î³ induced the expression of IL­6, IL­8, TARC and MDC in a dose­dependent manner through NF­κB and Janus kinase/signal transducers and activators of transcription (JAK/STAT) activation. Notably, treatment with RAME significantly suppressed TNF-α/IFN-γ-induced expression of IL­6, IL­8, TARC, and MDC. In addition, RAME treatment inhibited the activation of NF­κB and the JAK/STAT pathway in TNF­α/IFN­Î³­induced HaCaT cells. These results suggest that RAME decreases the production of chemokines and pro­inflammatory cytokines by suppressing the NF­κB and the JAK/STAT pathways. Consequently, RAME may potentially be used for treatment of atopic dermatitis.

Physalis peruviana L. inhibits airway inflammation induced by cigarette smoke and lipopolysaccharide through inhibition of extracellular signal-regulated kinase and induction of heme oxygenase-1.

Physalis peruviana L. (PP) is a medicinal herb that has been confirmed to have several biological activities, including anticancer, antioxidant and anti-inflammatory properties. The aim of the present study was to evaluate the protective effect of PP on cigarette smoke (CS)- and lipopolysaccharide (LPS)-induced pulmonary inflammation. Treatment with PP significantly reduced the influx of inflammatory cells in the bronchoalveolar lavage fluid (BALF) and lung of mice with CS- and LPS-induced pulmonary inflammation. PP also decreased the levels of reactive oxygen species (ROS) and pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the BALF. PP effectively attenuated the expression of monocyte chemoattractant protein-1 (MCP-1) and the activation of extracellular signal-regulated kinase (ERK) in the lung. In addition, nuclear factor erythroid 2-related factor 2 (Nrf2) activation and heme oxygenase-1 (HO-1) expression were increased by PP treatment. In an in vitro experiment, PP reduced the mRNA expression of TNF-α and MCP-1, and the activation of ERK in CS extract-stimulated A549 epithelial cells. Furthermore, PP increased the activation of Nrf2 and the expression of HO-1 in A549 cells. These findings suggest that PP has a therapeutic potential for the treatment of pulmonary inflammatory diseases, such as chronic obstructive pulmonary disease.