Effects of Sanchi extract on the activation and proliferation of murine lymphocytes and NO secretion by peritoneal macrophages in vitro

The aim of this study is to elucidate the molecular and cellular mechanisms underlying the immunosuppressive effect of Sanchi extract （SE） via investigating the effects of SE on the activation and proliferation of murine lymphocytes and NO secretion by peritoneal macrophages in vitro. ConA was used to activate lymphecytes, and expression of CD69 on T cells and CFSE labeled cell division were detected by flow cytometry. Murine peritoneal macrophages were stimulated with LPS or lymphocytes culture supernate （LCS） and the concentration of NO was determined by Griess reagent assay. After 6 h of culture, SE ranging from 50 to 100μg/ml downregulated CD69 expression on ConA-activated T cells, while SE ranging from 12.5 to 100μg/ml inhibited the proliferative response of lymphocytes to ConA. Additionally, SE （12.5-100μg/ml） inhibited secretion of NO by peritoneal macrophages stimulated by LPS or LCS. This study reveals that SE inhibits the activation and proliferation of routine lymphocytes and NO secretion by peritoneal macrophages.

Inflammatory Changes in Paravertebral Sympathetic Ganglia in Two Rat Pain Models

Injury to peripheral nerves can lead to neuropathic pain, along with well-studied effects on sensory neurons, including hyperexcitability, abnormal spontaneous activity, and neuroinflammation in the sensory ganglia. Neuropathic pain can be enhanced by sympathetic activity. Peripheral nerve injury may also damage sympathetic axons or expose them to an inflammatory environment. In this study, we examined the lumbar sympathetic ganglion responses to two rat pain models： ligation of the L5 spinal nerve, and local inflammation of the L5 dorsal root ganglion （DRG）, which does not involve axotomy. Both models resulted in neuroinflammatory changes in the sympathetic ganglia, as indicated by macrophage responses, satellite glia activation, and increased numbers of T cells, along with very modest increases in sympathetic neuron excitability （but not spontaneous activity） measured in ex vivo recordings. The spinal nerve ligation model generally caused larger responses than DRG inflammation. Plasticity of the sympathetic system should be recognized in studies of sympathetic effects on pain.

Resolution of inflammation and repair after ischemic brain injury

After ischemic stroke, proinflammatory molecules known as danger-associated molecular patterns (DAMPs) originating from damaged brain cells recruit and activate immune cells (neutrophils, macrophages, lymphocytes) further eliciting innate and adaptive immunity. During the acute phase from day 1 to day 3 of the stroke onset, macrophages play a major role in the progression of inflammation, promoting the destruction of brain tissue. During the recovery phase, from day 3~4 to day 7 after stroke onset, infiltrating macrophages switch to repairing macrophages, which clear the DAMPs and promote tissue repair by producing neurotrophic factors. Adaptive immunity during the late or chronic phase (> day 7) of stroke has not been well investigated. Recent studies have also indicated that antigen-specific T cells, especially regulatory T cells (Tregs), play major roles in neural repair. This review focuses mainly on the resolution of inflammation and tissue repair by macrophages and Tregs.