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Herbal medicines have been used as a treatment option for rheumatic disease (RD), but they often produce liver enzyme abnormality. This study examines the incidence of herb-induced liver injury (HILI) and the relationship between risk factors and liver enzyme abnormality (LEA) in inpatients with RD. HILI was analyzed using the Roussel Uclaf causality assessment method liver injury criteria and causality assessment. Multivariable analysis was performed to assess the relationship between patient characteristics and LEA in RD. The features of LEA were also examined in each RD. Among 352 patients included in this study, 105 patients showed LEA on admission, of which 6 had fulfilled the Roussel Uclaf causality assessment method criteria. The incidence risks of LEA and HILI were 12.55% and 0.58%, respectively. Multivariable analysis showed that LEA on admission and occasional use of alcohol could be risk factors for LEA on follow-up. In an additional analysis with each RD, all rheumatoid arthritis patients with LEA were taking nonsteroidal anti-inflammatory drugs, steroids, and disease-modifying antirheumatic drugs, and 4 out of 5 gout patients with LEA were taking steroids. The use of herbal medicine in RD is relatively safe. However, regular monitoring of liver enzyme tests and examination of alcohol consumption are required.

Background Immunodysregulation polyendocrinopathy enteropathy X-linked syndrome (IPEX) is a lethal autoimmune disease caused by mutations in the Foxp3 gene scurfin (scurfy). Immunosuppressive therapy for IPEX patients has been generally ineffective and has caused severe side effects, however curcumin has shown immune regulation properties for inflammatory diseases, such as rheumatoid arthritis, psoriasis, and inflammatory bowel diseases without side effects. Objective The aim of this study was to investigate whether curcumin would attenuate symptoms of IPEX in mouse model and would prolong its survival period. Methods C57BL/6 mice were separated into scurfy or wild-type litter mate groups by genotyping, and each group subsequently was separated into 2 subgroups that were fed a 1% curcumin containing or normal diet from the last day of breast-feeding. After weaning, pups were fed either a 1% curcumin containing or normal diet until all scurfy mice die for survival data. To elucidate immune cell proportions in spleen and lymph nodes, cells were analyzed by flowcytometry. Cellular cytokine production was accessed to investigate the effects of curcumin in T cell differentiation in vitro. Results Scurfy mice fed a 1% curcumin diet survived 4.0-fold longer compared to scurfy (92.5 days) mice fed a normal diet (23 days). A curcumin diet decreased all of the Th1/Th2/Th17 cell populations and attenuated diverse symptoms such as splenomegaly in scurfy mice. In vitro experiments showed that curcumin treatment directly decreased the Th1/Th2/Th17 cytokine production of IFN-γ, IL-4, and IL-17A in CD4+ T cells. Conclusions Curcumin diet attenuated the scurfy-induced immune disorder, a model of IPEX syndrome, by inhibiting Th1/Th2/Th17 responses in mice. These results have implications for improving clinical therapy for patients with IPEX and other T cell related autoimmune diseases.

Taxilli Ramulus has been shown have antioxidant and anti-inflammatory activities. Cisplatin is the most active cytotoxic anti-cancer drugs. However, the nephrotoxicity of cisplatin limits its use as a therapeutic. In the present study, we examined whether Taxilli Ramulus could protect against cisplatin induced acute renal failure in mice. Taxilli Ramulus were administrated orally once a day for 3 days (150 or 300 mg/kg body wt). After 3 days, all groups of mice received a single dose of cisplatin (25 mg/kg (body wt)) intraperitoneally. Taxilli Ramulus treatment ameliorated renal dysfunction 72 h after cisplatin injection. Taxilli Ramulus treated group had significantly reduced levels of proinflammatory cytokines when compared to the control group. These results show that Taxilli Ramulus is a potent herbal medicine that can reduce cisplatin nephrotoxicity. It also demonstrates that Taxilli Ramulus can prevent the renal toxic effects caused by cisplatin.

The aim of this study was to determine of the effect of casticin, as an anti-inflammatory agent, on an acute lung inflammation in vivo model established through exposure to cigarette smoke (CS). Casticin is a phytochemical from Vitex species such as Vitex rotundifolia and Vitex agnus-castus that was recently shown to exert an anti-inflammatory effect in vivo. To demonstrate the effects of casticin, C57BL/6 mice were whole-body exposed to mainstream CS or fresh air for two weeks and treated with 1, 2, and 10mg/kg casticin via an i.p. injection. Immune cell infiltrations and cytokine productions were assessed from bronchoalveolar lavage Fluid (BALF), and lung histological analysis was performed. Treatment with casticin was observed to significantly inhibit the numbers of total cells, neutrophils, macrophages, and lymphocytes and reduce the levels of proinflammatory cytokines and chemokines in the BALF. In addition, casticin significantly decreased the infiltration of peribronchial and perivascular inflammatory cells and the epithelium thickness. The results of this study indicate that casticin has significant effects on the lung inflammation induced by CS in a mouse model. According to these outcomes, casticin may have therapeutic potential in inflammatory lung diseases, such as chronic obstructive pulmonary disease (COPD).

In the field of Oriental medicine, the root of Paeonia lactiflora (Paeoniae Radix) has been prescribed usually to treat the common cold, and it was thought to alleviate upper respiratory infection or nasal inflammation. Monocyte chemotactic proteins (MCP)-1 and MCP-3 are known as the most potent chemokines to mediate allergic inflammation. The object of the study was to investigate the effect of Paeoniae Radix on the release of the chemokines such as MCP-1 and MCP-3. To detect the secretion of MCPs, an enzyme-linked immunosorbent assay was performed for human nasal mucosal fibroblasts after stimulation with several cytokines such as tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and interleukin-1beta (IL-1beta). The secretion of MCP-1 was increased after stimulation with TNF-alpha or IL-1beta treatment. Co-treatment of TNF-alpha and IFN-gamma, or IL-1beta and IFN-gamma increased the secretion of MCP-1 and MCP-3. Paeoniae Radix was tested with inflammatory cytokines, and the results showed that the Paeoniae Radix significantly decreased the secretion of MCP-1 and MCP-3. In our study, Paeoniae Radix may play an important role in nasal inflammation with a modulation of MCP-1 and MCP-3.