Upregulation of VDR-associated lncRNAs in Schizophrenia.

Vitamin D receptor (VDR) signaling has been found to contribute to the pathology of numerous neuropsychiatric diseases including schizophrenia. Notably, VDR signaling has a functional relationship with many long non-coding RNAs (lncRNAs) such as SNHG6, LINC00346 and LINC00511. We calculated expression of these lncRNAs in the venous blood of patients with schizophrenia versus healthy individuals. Expression of SNHG6 was significantly higher in cases versus controls (posterior beta = 0.552, adjusted P value < 0.0001). This pattern of expression was detected in both men (posterior beta = 0.556, adjusted P value < 0.0001) and women (posterior beta = 0.31, adjusted P value = 0.005). Expression of LINC00346 was also higher in cases versus controls (posterior beta = 0.497, adjusted P value < 0.0001) and in distinct sex-based comparisons (posterior beta = 0.451, adjusted P value = 0.009 among men and posterior beta = 0.214, P value = 0.004 among women). Expression of LINC00511 was higher in cases versus controls (posterior beta = 0.318, adjusted P value = 0.01). While sex-based comparisons revealed significant difference in expression of LINC00511 among female subgroups (posterior beta = 0.424, adjusted P value = 0.016), such comparison showed no difference among male cases and male controls (adjusted P value = 0.295). The expression levels of SNHG6 distinguished patients with schizophrenia from controls, with AUC = 0.932. LINC00346 and LINC00511 distinguished between the two groups with AUC values of 0.795 and 0.706, respectively. Therefore, these lncRNAs might be used as markers for schizophrenia.

Anti-inflammatory and immune-modulatory impacts of berberine on activation of autoreactive T cells in autoimmune inflammation.

Autoreactive inflammatory CD4+ T cells, such as T helper (Th)1 and Th17 subtypes, have been found to associate with the pathogenesis of autoimmune disorders. On the other hand, CD4+ Foxp3+ T regulatory (Treg) cells are crucial for the immune tolerance and have a critical role in the suppression of the excessive immune and inflammatory response promoted by these Th cells. In contrast, dendritic cells (DCs) and macrophages are immune cells that through their inflammatory functions promote autoreactive T-cell responses in autoimmune conditions. In recent years, there has been increasing attention to exploring effective immunomodulatory or anti-inflammatory agents from the herbal collection of traditional medicine. Berberine, an isoquinoline alkaloid, is one of the main active ingredients extracted from medicinal herbs and has been shown to exert various biological and pharmacological effects that are suggested to be mainly attributed to its anti-inflammatory and immunomodulatory properties. Several lines of experimental study have recently investigated the therapeutic potential of berberine for treating autoimmune conditions in animal models of human autoimmune diseases. Here, we aimed to seek mechanisms underlying immunomodulatory and anti-inflammatory effects of berberine on autoreactive inflammatory responses in autoimmune conditions. Reported data reveal that berberine can directly suppress functions and differentiation of pro-inflammatory Th1 and Th17 cells, and indirectly decrease Th cell-mediated inflammation through modulating or suppressing other cells assisting autoreactive inflammation, such as Tregs, DCs and macrophages.