Angiogenesis activity of Jatropha curcas L. latex in cream formulation on wound healing in mice.

AIM: The aim of this research was to determine the angiogenesis activity of Jatropha curcas latex in cream formulation on CD34 immune expression during wound healing phase in mice skin. MATERIALS AND METHODS: Amount of 36 2-month-old male mice were used between 30 and 40 g. To surgical procedures, wound skin incision was performed 2.0 cm in length until subcutaneous on the paravertebral of each animal. The treatment was carried under locally anesthetized with procaine cream. All mice were divided into four groups, namely the base cream as control group (A), sulfadiazine 0.1% cream (B), Jatropha curcas latex cream 10% (C), and J. curcas latex cream 15% (D). All groups were treated entire surface of wound. All experiments were performed twice a day for 10 days. Experiments were terminated on days 3, 7, and 10, respectively. The wound healing was assayed in stained histological section in immunohistochemical of the wounds. The CD34 expression was investigated under a microscope. RESULTS: The results showed that the cream from 10% and 15% latex J. curcas revealed moderate immune reaction to CD34 on days 3 and 7 in wound healing of mice skin. CONCLUSION: We concluded that the cream from 10% and 15% latex J. curcas has potential as angiogenesis activity in wound healing of mice skin.

Anti-inflammatory activity of Jatropha curcas Linn. latex in cream formulation on CD68 expression in mice skin wound.

AIM: The purpose of the present study was to determine the potential of Jatropha curcas latex in the cream formulation on CD68 immune expression (macrophages) during inflammatory phase wound healing process in mice skin. MATERIALS AND METHODS: Amount of 12 two-months-old male mice were used between 30 and 40 g. To surgical procedures, wound skin incision was performed 2.0 cm in length until subcutaneous on the paravertebral of each animal. The treatment was carried under locally anesthetized with procaine cream. The mice were allotted into four groups of each, entire surface of each group wound covered by base cream control, sulfadiazine 0.1% cream, J. curcas latex cream 10% and, 15%, respectively. All experiments were performed twice a day for 3 days. The wound healing was assayed in stained histological sections in immunohistochemical of the wounds. CD68 expression was investigated under a microscope. RESULTS: The results showed that the cream from the 10% and 15% latex of J. curcas revealed moderate immune reaction to CD68 on wound healing. CONCLUSION: We concluded that the latex cream of J. curcas possesses anti-inflammatory activity in wound healing process of mice skin.

Dynamic Changes of Microglia/Macrophage M1 and M2 Polarization in Theiler's Murine Encephalomyelitis.

Microglia and macrophages play a central role for demyelination in Theiler's murine encephalomyelitis (TME) virus infection, a commonly used infectious model for chronic-progressive multiple sclerosis. In order to determine the dynamic changes of microglia/macrophage polarization in TME, the spinal cord of Swiss Jim Lambert (SJL) mice was investigated by gene expression profiling and immunofluorescence. Virus persistence and demyelinating leukomyelitis were confirmed by immunohistochemistry and histology. Electron microscopy revealed continuous myelin loss together with abortive myelin repair during the late chronic infection phase indicative of incomplete remyelination. A total of 59 genes out of 151 M1- and M2-related genes were differentially expressed in TME virus-infected mice over the study period. The onset of virus-induced demyelination was associated with a dominating M1 polarization, while mounting M2 polarization of macrophages/microglia together with sustained prominent M1-related gene expression was present during the chronic-progressive phase. Molecular results were confirmed by immunofluorescence, showing an increased spinal cord accumulation of CD16/32(+) M1-, arginase-1(+) M2- and Ym1(+) M2-type cells associated with progressive demyelination. The present study provides a comprehensive database of M1-/M2-related gene expression involved in the initiation and progression of demyelination supporting the hypothesis that perpetuating interaction between virus and macrophages/microglia induces a vicious circle with persistent inflammation and impaired myelin repair in TME.

Limited role of regulatory T cells during acute Theiler virus-induced encephalitis in resistant C57BL/6 mice.

BACKGROUND: Theiler's murine encephalomyelitis virus (TMEV) infection represents a commonly used infectious animal model to study various aspects of the pathogenesis of multiple sclerosis (MS). In susceptible SJL mice, dominant activity of Foxp3(+) CD4(+) regulatory T cells (Tregs) in the CNS partly contributes to viral persistence and progressive demyelination. On the other hand, resistant C57BL/6 mice rapidly clear the virus by mounting a strong antiviral immune response. However, very little is known about the role of Tregs in regulating antiviral responses during acute encephalitis in resistant mouse strains. METHODS: In this study, we used DEREG mice that express the diphtheria toxin (DT) receptor under control of the foxp3 locus to selectively deplete Foxp3(+) Tregs by injection of DT prior to infection and studied the effect of Treg depletion on the course of acute Theiler's murine encephalomyelitis (TME). RESULTS: As expected, DEREG mice that are on a C57BL/6 background were resistant to TMEV infection and cleared the virus within days of infection, regardless of the presence or absence of Tregs. Nevertheless, in the absence of Tregs we observed priming of stronger effector T cell responses in the periphery, which subsequently resulted in a transient increase in the frequency of IFNγ-producing T cells in the brain at an early stage of infection. Histological and flow cytometric analysis revealed that this transiently increased frequency of brain-infiltrating IFNγ-producing T cells in Treg-depleted mice neither led to an augmented antiviral response nor enhanced inflammation-mediated tissue damage. Intriguingly, Treg depletion did not change the expression of IL-10 in the infected brain, which might play a role for dampening the inflammatory damage caused by the increased number of effector T cells. CONCLUSION: We therefore propose that unlike susceptible mice strains, interfering with the Treg compartment of resistant mice only has negligible effects on virus-induced pathologies in the CNS. Furthermore, in the absence of Tregs, local anti-inflammatory mechanisms might limit the extent of damage caused by strong anti-viral response in the CNS.