Mango (Mangifera indica L.) is a succulent tropical fruit. Bioactive phytochemical investigation has been carried out to the leaves of mango. Three new benzophenone glycosides, along with 14 known compounds, were purified and identified. The novel benzophenones were elucidated to be 2,4,4',6-tetrahydroxy-3'-methoxybenzophenone-3-C-β-d-glucopyranoside (1), 4,4',6-trihydroxybenzophenone-2-O-α-l-arabinofuranoside (7), and 4',6-dihydroxy-4-methoxybenzophenone-2-O-(2″),3-C-(1″)-1″-desoxy-α-l-fructofuranoside (11). The α-glucosidase inhibitory, NO production inhibitory, and antioxidant activities were assessed for the purified benzophenones and triterpenoids. Some benzophenones showed moderate α-glucosidase and NO inhibitory activities. The IC value of the α-glucosidase inhibitory of isolated compounds 1, 13, and 14 were 284.93 ± 20.29, 239.60 ± 25.00, and 297.37 ± 8.12 μM, respectively. Most compounds showed moderate effects to reduce the NO content in 50 and 100 μM. The above results of bioactivity powerfully demonstrated the phytochemicals from mango, especially benzophenones, probably partially rational for its antidiabetes and anti-inflammatory.
As a new generation of treatment, tumor immunotherapy targeting tumor-associated antigens (TAA) has attracted widespread attention. The survivin antigen belongs to TAA. It is a key inhibitor of apoptosis and a key regulator of cell cycle progression; furthermore, it may be a candidate target for tumor therapy. In addition, studies have confirmed that granulocyte-macrophage colony-stimulating factor (GM-CSF) and CCL17 significantly affect local anti-tumor immunity in the tumor microenvironment. The mouse survivin gene was screened by BIMAS and SYFPEITHI to obtain the highest scored mouse survivin epitope peptide, which was synthesized into a peptide vaccine to immunize normal mice. Subsequently, spleen lymphocytes were isolated to induce survivin-specific cytotoxic T lymphocytes (CTL). Next, genetic engineering was used to construct the B16F10 cell line that stably expressed CCL17 and GM-CSF genes. A mouse melanoma model was used to observe the effects of the combination of the three on tumor volume and tumor weight. In-vitro survivin-specific CTL combined with CCL17 gene had a stronger inhibitory effect on B16F10 cells, while combined GM-CSF gene did not enhance the inhibitory effect of CTL on B16F10 cells. In-vivo experiments demonstrated that survivin-specific CTL combined with GM-CSF and CCL17 genes can inhibit the growth of mouse melanoma. HE staining and immunohistochemistry showed that the tumor had more necrotic cells and more infiltrating lymphocytes. The results showed that survivin-specific CTL combined with CCL17 and GM-CSF genes could inhibit tumor growth better.
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