Phytochemical and biological studies of the methanolic extracts from Ganoderma lucidum (Polyporaceae) have led to the identification and isolation of a new lanostane triterpenoid, ganosidone A (1), and its eight known derivatives (2-9). The structure of new compound was determined by HREIMS, 1D and 2D NMR experiments and by comparing the acquired physicochemical data with the published values. All the compounds were evaluated for cancer chemopreventive potential based on their ability to inhibit nitric oxide (NO) production induced by lipopolysaccharides (LPS) in mouse macrophage RAW 264.7 cells in vitro. Notably, at a concentration of 50 M, compounds 4 and 7 inhibited NO production by 86.5 % and 88.2 %, respectively.
Colorectal cancer is one of the life-threatening ailments causing high mortality and morbidity worldwide. Despite the innovation in medical genetics, the prognosis for metastatic colorectal cancer in patients remains unsatisfactory. Recently, lichens have attracted the attention of researchers in the search for targets to fight against cancer. Lichens are considered mines of thousands of metabolites. Researchers have reported that lichen-derived metabolites demonstrated biological effects, such as anticancer, antiviral, anti-inflammatory, antibacterial, analgesic, antipyretic, antiproliferative, and cytotoxic, on various cell lines. However, the exploration of the biological activities of lichens’ metabolites is limited. Thus, the main objective of our study was to evaluate the anticancer effect of secondary metabolites isolated from lichen (Usnea barbata 2017-KL-10) on the human colorectal cancer cell line HCT116. In this study, 2OCAA exhibited concentration-dependent anticancer activities by suppressing antiapoptotic genes, such as MCL-1, and inducing apoptotic genes, such as BAX, TP53, and CDKN1A(p21). Moreover, 2OCAA inhibited the migration and invasion of colorectal cancer cells in a concentration-dependent manner. Taken together, these data suggest that 2OCAA is a better therapeutic candidate for colorectal cancer.
Inflammation mediated by the innate immune system is the organism’s protective mechanism against infectious environmental risk factors. Uncontrolled acute inflammation can become chronic, contributing to various chronic inflammatory diseases such as arthritis, asthma, autoimmune
diseases, and atherosclerosis. Although microalgae are increasingly receiving attention as a source of bioactive molecules with therapeutic potential for various human diseases, the underlying mechanisms are not yet well understood. In the present study, we investigated the molecular mechanisms
underlying the anti-inflammatory and anti-aging activities of ethanol extracts of Antarctic freshwater microalga Micractinium simplicissimum. Using RAW 264.7 macrophages, microalgal extracts exerted anti-inflammatory activity by regulating the major inflammatory indicators including
cyclooxy-genase (COX)-2, interleukin (IL)-6, inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF)-α and nitric oxide (NO). Besides, we observed the anti-aging activity of the microalgal extract by suppressing MMP-1 production in human dermal fibroblast. Taken together,
these data suggest that anti-inflammatory and anti-aging activities of Antarctic freshwater microalga, Micractinium simplicissimum, can provide new clues to understanding the molecular link between inflammation and diseases, and be a potential anti-inflammatory agent.
Colorectal cancer (CRC) is a deadly disease regardless of sex, and a few therapeutic approaches have been fully developed at advanced stages, even if some strategies have durable clinical benefits, such as immunotherapy and chemotherapy. Ganoderma lucidum has been recognized as an organism that suppresses tumors and inflammation; however, the molecular mechanisms induced by a triterpenoid in Ganoderma lucidum, Lucidumol A, have not yet been fully explored in CRC and inflammatory responses. To this end, we extracted Lucidumol A from Ganoderma lucidum and analyzed its anticancer effect and anti-inflammatory potential in CRC cell lines and RAW264.7 macrophage-derived cell lines, respectively. A series of in vitro experiments including cell survival, wound healing, and migration assays were performed to determine the role of Lucidumol A in the CRC cell line. We also analyzed inflammatory responses using qRT-PCR, Western Blot, and ELISA in RAW 264.7 macrophaged-derived cell lines exposed to various concentrations of Lucidumol A. Lucidumol A efficiently suppressed the metastatic potential of CRC at very low concentrations. Furthermore, significant anti-inflammatory activities were observed in Lucidumol A-treated RAW264.7 cells through modulation of inflammation-associated marker genes and cytokines. In conclusion, Lucidumol A plays an important role in Ganoderma lucidum-dependent tumor suppression and anti-inflammation, suggesting different strategies to treat CRC patients, and other diseases evoked by proinflammatory cytokines, despite the need to explore further its mechanism of action.
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