What medicinal functions does cordycepin have?

　　Cordycepin mainly comes from two sources: chemical synthesis and extraction and purification from Cordyceps militaris. In the early 1950s, it was reported that monomers could be obtained by extraction, and in the 1960s, synthetic products were also reported. The route design for chemical synthesis of cordycepin mainly involves replacing the CO bond at the 3' position of the deoxyribose ring to form a 2', 3'-epoxydeoxyribose structure, followed by regional stereoselective ring opening and direct synthesis of 3-deoxyribose derivatives. Pioneering results have been achieved in applied research in areas such as the inhibitory effect of viral transcriptase and infection; the effect on the production of interleukin-10 by human peripheral blood mononuclear cells; anti-leukemia activity and mechanism of action... etc.

　　Although the efficacy of cordycepin has been studied in depth at home and abroad, the industrial extraction of cordycepin has always been a problem because the cordycepin content in wild cordyceps and artificial cordyceps, including cordyceps militaris, is extremely low and unstable, making extraction difficult. After several years of research, experts from various fields have successfully realized the industrial extraction of cordycepin and successfully developed a series of cordycepin lozenges from Dacheng Cao. This has achieved a milestone leap in the scientific utilization of cordyceps and cordycepin. China has finally been at the forefront of the world in the scientific research and utilization of cordycepin for more than half a century since 1957.

　　Medicinal valueEditImmune regulation

　　Researchers found that cordycepin has immunomodulatory effects. It can greatly increase the secretion of IL-10 and the expression of IL-10 mRNA in human peripheral blood monocytes. At the same time, cordycepin has an inhibitory effect on the phytohemagglutinin that induces the production of IL-2 and the expansion of peripheral blood monocytes. Anti-IL-10 neutral antibodies cannot completely prevent the inhibitory effect of cordycepin on IL-2 production. Under the action of cordycepin, mature dendritic cells can induce the proliferation of regulatory T cells, inhibit cell division, promote cell differentiation, change the distribution of material structures on the cell membrane, and promote the transformation of T lymphocytes. It can also improve the phagocytic function of the body's mononuclear macrophage system and activate macrophages to produce cytotoxins to directly kill cancer cells. In addition, cordycepin can also inhibit protein kinase activity, resist the cleavage of sugar groups by nucleoside phosphorylase, and regulate humoral immunity. In experiments to study the anti-delayed-type hypersensitivity reaction of domestic cordycepin in mice and its immune mechanism, it was shown that cordycepin may exert a significant inhibitory effect on contact dermatitis in mice caused by delayed-type hypersensitivity reaction through other immunomodulatory effects. This effect is related to the dose of the drug, and there is no obvious toxic effect on spleen tissue.

　　Anti-tumor

　　The inhibitory effect of cordycepin on tumors has always been a focus of scientists. The study found that the median survival time of mice inoculated with Ehrlich ascites cancer by dermal injection with cordycepin was extended to 60 days, while that of the control group was only 19 days. This shows that cordycepin has a significant inhibitory effect on Ehrlich ascites cancer in mice and can significantly extend the survival time of mice inoculated with Ehrlich ascites cancer. Other studies have shown that cordycepin has a significant inhibitory effect on human nasopharyngeal carcinoma KB cells and human cervical cancer HeLa cells. Scientists speculate that cordycepin may have three tumor-inhibiting mechanisms: first, the free hydroxyl group of cordycepin can penetrate into the DNA of tumor cells and act; second, it inhibits the phosphorylation of nucleosides or nucleotides to generate diphosphate and triphosphate derivatives, thereby inhibiting the synthesis of nucleic acids in tumor cells; third, it blocks the process of amination of xanthine to form guanylic acid.