Copaifera oleoresin is one of the most used natural products in popular medicine all over the world. Among other effects (i.e., anti-inflammatory, antinociceptive, microbicidal) one of the most well-known is its wound healing capacity. However, the mechanism by which the oleoresin presents its effect is still not clear. In this study, our aim was to evaluate the wound healing capacity of oleoresin obtained from Copaifera paupera, its mechanism of action and identify its major components. For these purposes, diabetic Swiss Webster mice were topically treated with oleoresin (100, 150 or 200 mg/kg) for 14 consecutive days after an excision was performed in the back of the mice. Cytokines, wound retraction and histological evaluation were conducted at 3, 7 and 10 days (for cytokines); 0, 3, 7, 10 and 14 days (for wound retraction); and 7 and 14 days (for histological evaluation). Our data indicate that oleoresin significantly reduced production of MCP-1 and TNF-α at days 7 and 10 post-excision and increased IL-10 production at both days. All treatments demonstrated an effect similar or higher to that in collagenase-treated mice. Histological evaluations demonstrated that higher dose treatment resulted in better resolution and closure of the wound and higher levels of collagen deposition and indexes of re-epithelialization even when compared with the collagenase-treated group. The treatment with oleoresin from Copaifera paupera demonstrated that it is even better than an ointment routinely used for improvement of wound healing, suggesting this oleoresin as an option for use in diabetic patients.
Malignancies of the central nervous system include primary brain tumors and brain metastases, the latter being the major cause of intracranial neoplasms in adults. Although prostate cancer (PCa) brain metastases are not the most common source, recent data show that the relevance of prostate cancer brain metastases (PCBM) cannot be neglected. In this review, we focus on the molecular repertory as well as on the phenotypical similarities between PCBM and primary PCa, such as the cellular evolution and the maintenance of androgen-receptor expression. Moreover, the simultaneous occurrence of PCBM with other PCa metastatic sites and the significance of the clinical heterogeneity of the disease are also discussed. In addition, a potential relationship between the heterogeneous behavior exhibited by PCBM and the co-occurrence of malignant cell clusters with distinct genetic profiles is also hypothesized, as well as the prominent role of astrocytes in the establishment of PCBM.
Tumor establishment, growth, and survival are supported by interactions with microenvironment components. Here, we investigated whether the interactions between prostate cancer cells and cortical astrocytes are associated to a potential role for astrocytes in tumor establishment. We demonstrate that astrocytes interact in vitro with prostatic cancers cells derived from different metastatic sites. Astrocytes and their secreted extracellular matrix, stimulate DU145 cell (a brain-derived prostate tumor cell line) proliferation while inhibiting cell death and modulating the expression of several genes related to prostate cancer progression, suggesting the activation of EMT process in these cells. In contrast, DU145 cells and their conditioned medium inhibited cell proliferation and induced cell death of astrocytes. On the other hand, the astrocytes were unable to significantly induce an increment of LNCaP cell (a lymph node-derived prostate tumor cell line) proliferative activity. In addition, LNCaP cells were also unable to induce cell death of astrocytes. Thus, we believe that DU145 cells, but not LNCaP cells, present an even more aggressive behavior when interacting with astrocytes. These results provide an important contribution to the elucidation of the cellular mechanisms involved in the brain microenvironment colonization.
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