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Cordyceps militaris is a medicinal mushroom in Asia in the 21st century, which cordycepin is a significant bioactive compound. This study, investigated the effect of culture conditions and vegetable seed extract powder as a supplementary source of animal-free nitrogen on the production of cordycepin by C. militaris in liquid surface culture. The highest cordycepin production was observed under soybean extract powder (SBEP) conditions, and 80 g L−1 of SBEP supplementation increased cordycepin production to 2.52 g L−1, which was greater than the control (peptone). Quantitative polymerase chain reaction was used to examine the transcription levels, and the results showed that supplementing with SBEP 80 g L−1 significantly increased the expression of genes associated with the carbon metabolic pathway, amino acid metabolism, and two key genes involved in the cordycepin biosynthesis (cns1 and NT5E) compared to peptone-supplemented culture. Under optimal culture conditions, the model predicted a maximum response of cordycepin production of 2.64 g L−1 at a working volume of 147.5 ml, an inoculum size of 8.8% v/v, and a cultivation time of 40.0 days. This optimized culture condition could be used to increase cordycepin production in large-scale bioreactors. Additional research can be conducted to assess the economic viability of this process. [ABSTRACT FROM AUTHOR]

Background/Aim: Mesenchymal stem cells (MSCs) have been employed for therapeutic applications of various degenerative diseases. However, the major concern is MSC aging during the in vitro cultivation. Thus, the approach to delay MSC aging was examined in this research by focusing on the expression of Sirtuin 1 (SIRT1), a key anti-aging marker. Materials and Methods: Cordycepin, a bioactive compound derived from Cordyceps militaris, was used to up-regulate SIRT1 and maintain stemness of MSCs. Upon treatment with cordycepin, MSCs were investigated for cell viability, doubling time, key gene/protein expression, galactosidase-associated senescence assay, relative telomere length, and telomerase expression. Results: Cordycepin significantly increased the expression of SIRT1 in MSCs by activating the adenosine monophosphate activated protein kinase (AMPK)-SIRT1 signalling pathway. Moreover, cordycepin maintained the stemness of MSCs by deacetylating SRY-box transcription factor 2 (SOX2) via SIRT1, and cordycepin delayed cellular senescence and aging of MSCs by enhancing autophagy, inhibiting the activity of senescence-associated-galactosidase, maintaining proliferation rate, and increasing telomere activity. Conclusion: Cordycepin could be used to increase SIRT1 expression in MSCs for anti-aging applications. [ABSTRACT FROM AUTHOR]

Breast cancer (BC) is a major type of cancer found in women worldwide, accounting for more than 25% of all females diagnosed as BC patients. The BC treatment still needs to be highly effective with few adverse effects on the rest of the body. This study's objective was to investigate how hispolon enhanced anticancer activities and examine the underlying processes in human breast cancer cells. Hispolon was used to treat the HTB-26 cell lines. We investigated cell viability, intracellular reactive oxygen species (ROS) production, immunofluorescence straining, MDC assay, and RT-PCR. According to the findings, hispolon inhibited HTB-26 cells from proliferating and caused them to undergo apoptosis. When the mechanism of action of hispolon was investigated, it was discovered that BCL-2 expression was downregulated while pro-apoptotic genes including caspase-3, caspase-9, and BAX were upregulated. The level of intracellular ROS was also shown to be increased by hispolon, and the expression of antioxidant genes including SOD, GPX, and Catalase was found to be downregulated. The increase in the confocal fluorescence image of LC3I/II and the identification of upregulated autophagy-related genes, such as LC3I/II, ATG5, ATG10, and ATG12, served as indicators of the activation of autophagy. Therefore, our findings showed that hispolon had great potential for being an effective therapeutic agent and could cause cell death in breast cancer cells. [ABSTRACT FROM AUTHOR]