Secondary mechanisms, including inflammation and microglia activation, serve as targets for the development and application of pharmacological strategies in the management of spinal cord injury (SCI). Tetramethylpyrazine (TMP), an active ingredient of Ligusticum wallichii (chuanxiong), has shown anti-inflammatory and neuroprotective effects against SCI. However, it remains uncertain whether the inflammation-suppressive effects of TMP play a modulatory role over microglia activation in SCI. The present study investigated the effects of TMP on microglia activation and pro-inflammatory cytokines in spinal cord compression injury in mice. For a real-time PCR measurement of pro-inflammatory cytokines, SCI was induced in mice by the clip compression method (30 g force, 1 min) and TMP (15 or 30 mg/kg, i.p.) was administered once, 30 minutes before the SCI induction. For immunohistochemistry, TMP (30 mg/kg, i.p.) treatment was given three times during the first 48 hours after the SCI. 30 mg/kg of TMP treatment reduced the up-regulation of TNF-α, IL-1β and COX-2 mRNA in the spinal tissue at four hours after the SCI induction. TMP also significantly attenuated microglia activation and neutrophil infiltration at 48 hours after the SCI induction. In addition, iNOS expression in the spinal tissue was attenuated with TMP treatment. These results suggest that TMP plays a modulatory role in microglia activation and may protect the spinal cord from or potentially delay secondary spinal cord injury.

Atopic dermatitis (AD) is a common inflammatory skin disorder mediated by inflammatory cells, such as macrophages and mast cells. Rifampicin is mainly used for the treatment of tuberculosis. Recently, it was reported that rifampicin has anti-inflammatory and immune-suppressive activities. In this study, we investigated the effect of rifampicin on atopic dermatitis in vivo and in vitro. AD was induced by treatment with 2, 4-dinitrochlorobenzene (DNCB) in NC/Nga mice. A subset of mice was then treated with rifampicin by oral administration. The severity score and scratching behavior were alleviated in the rifampicin-treated group. Serum immunoglobulin E (IgE) and interleukin-4 (IL-4) levels were also ameliorated in mice treated with rifampicin. We next examined whether rifampicin has anti-atopic activity via suppression of mast cell activation. Rifampicin suppressed the release of β-hexosaminidase and histamine from human mast cell (HMC)-1 cultures stimulated with compound 48/80. Treatment with rifampicin also inhibited secretion of inflammatory mediators, such tumor necrosis factor-α (TNF-α) and prostaglandin D2 (PGD2), in mast cells activated by compound 48/80. The mRNA expression of cyclooxygenase 2 (COX-2) was reduced in the cells treated with rifampicin in a concentration-dependent manner. These results suggest that rifampicin can be used to treat atopic dermatitis.

The process of drug discovery and drug development consumes billions of dollars to bring a new drug to the market. Drug development is time consuming and sometimes, the failure rates are high. Thus, the pharmaceutical industry is looking for a better option for new drug discovery. Drug repositioning is a good alternative technology that has demonstrated many advantages over de novo drug development, the most important one being shorter drug development timelines. In the last two decades, drug repositioning has made tremendous impact on drug development technologies. In this review, we focus on the recent advances in drug repositioning technologies and discuss the repositioned drugs used for inflammatory diseases such as sepsis, asthma, and atopic dermatitis.

Objectives: In this case report, we will show the effectiveness of herbal medicine with neurofeedback treatment on social phobia. Methods: First, we diagnosed the patient by interview and questionnaire as having social phobia and suffering from anxiety, shaking and palpitation in public places and fear to meet new people. Beside, we examined the pattern of brainwaves by QEEG-8 system. Second, we treated the patient by herbal medicine with neurofeedback treatment for 4 months. Then we conducted new assessments by SCL-90-R, BDI, BAI and QEEG-8 system. Results: The patient's psychological and physiological symptoms were significantly improved. Conclusions: Herbal medicine with neurofeedback can be effective in the treatment of social phobia. Especially, it can be helpful to improve the patient's sensitivity to its physiological symptoms.

Atopic dermatitis is a chronic, inflammatory skin disorder associated with defective skin barrier and epidermal hyper reactivity. AD is a Th2 mediated allergic disease. GATA3 is a transcription factor that plays an important role in Th2 differentiation. In this study we investigated the per2 gene role and the expression of per2 related genes in atopic dermatitis. We established the atopic dermatitis animal model in per2 knock out and C57BL/6 by 2,4-dinitrochlorobenzene (DNCB). A subset of mice in both per2 knock out and C57BL/6 were treated with saline as control group. The skin lesions severity score was alleviated in per2 knock out mice DNCB group than wild type group. We examined the TNF-α mRNA expression in skin samples that showed that per2 knock out mice protected from DNCB induced inflammation than wild type mice. We next examined BMAL1 mRNA expression in skin samples that showed BMAL1 functioned as anti-inflammatory molecule in per2 knock out mice and levels are high than wild type mice and GATA3 expression levels were not initiated in per2 knock out mice than wild type mice. According to these results we hypothesized per2 knock out mice protected from allergic atopic dermatitis by increasing anti-inflammatory molecule BMAL1 through supressing GATA3.