The research team, including Dr. Kanako Mune, a doctoral student at the Graduate School of Pharmaceutical Sciences, Kyoto University, Takayuki Nakagawa, an associate professor at the Graduate School of Pharmaceutical Sciences, and Shuji Kaneko, a professor at the Graduate School of Pharmaceutical Sciences, said that numbness, which is similar to pain caused by sitting upright, is caused by nerve proteins near the skin. Was published in the British scientific journal "Scientific Reports", revealing that it is stimulated by active oxygen that is emitted after the resumption of professorship.
The sensation "numbness" that everyone has experienced, such as after sitting upright, occurs not only in diseases such as diabetes and peripheral neuropathy, but also in treatment with specific anticancer drugs, but the detailed mechanism is clear. No drug has been developed that is effective against this condition.
It is known that when blood flow is blocked and then resumed, a large amount of active oxygen is generated from cells.This research team focused on "TRPA1", a sensory nerve protein that causes pain in response to active oxygen.It was predicted that hypoxia due to decreased blood flow induces TRPA1 hypersensitivity, and that active oxygen generated by the resumption of blood flow stimulates TRPA1 and as a result, pain information is transmitted to the brain.
First, the hind legs on one side of the mouse were tied with a thread to stop the blood flow, and after a while, the thread was cut to resume the blood flow to reproduce "numbness". ..This behavior is seen as a phenomenon similar to the sensation of running, with the sensation of the legs disappearing after sitting upright for a long time.Furthermore, it was confirmed in the experiment that when TRPA1 is deficient in mice in this state, numbness is not felt. Numbness can be alleviated by the elimination of the TRPA1 gene, and by extension, drugs that capture and eliminate active oxygen, and TRPA1 inhibitors.
This study has revealed a part of the mechanism of numbness, but since it is thought that there is a different mechanism for numbness that does not go away even after a long time such as diabetes, it is stimulated by creating a pathological animal model of these diseases in the future. It is expected to develop a therapeutic drug that weakens the activity of TRPA1 activated by.