作為鈣離子滲透性的瞬時(shí)受體電位（TRP），5種通道（TRPV1~4和TRPM2）被不同的高溫激活，兩種通道（TRPV1和TRPV8）被低溫激活。越來(lái)越多的證據(jù)表明，TRPA1和TRPM8拮抗劑可預(yù)防順鉑、奧沙利鉑和紫杉醇誘導(dǎo)的線粒體氧化應(yīng)激、炎癥、冷痛和痛覺(jué)過(guò)敏。TRPV1在順鉑引起的感覺(jué)神經(jīng)元熱痛覺(jué)和機(jī)械異常中有應(yīng)答。TRPA1、TRPM8和TRPV2蛋白表達(dá)水平主要通過(guò)這些治療方法在背根（DRG）和三叉神經(jīng)節(jié)中增加。主要總結(jié)了5種溫度調(diào)節(jié)TRP通道（TRPA1、TRPM8、TRPV1、TRPV2和TRPV4）。

As members of the Ca²⁺ permeable transient receptor potential (TRP), five of the channels (TRPV1-4 and TRPM2) are activated by different heat temperatures, and two of the channels (TRPA1 and TRPM8) are activated by cold temperature. Accumulating evidences indicates that antagonists of TRPA1 and TRPM8 may protect against cisplatin, oxaliplatin, and paclitaxel-induced mitochondrial oxidative stress, inflammation, cold allodynia, and hyperalgesia. TRPV1 is responsible from the cisplatin-induced heat hyperalgesia and mechanical allodynia in the sensory neurons. TRPA1, TRPM8, and TRPV2 protein expression levels are mostly increased in the dorsal root (DRG) and trigeminal ganglia by these treatments. Five temperature-regulated TRP channels (TRPA1, TRPM8, TRPV1, TRPV2, and TRPV4) as novel targets for treating chemotherapy-induced neuralgia are summarized in this review.

國(guó)家自然科學(xué)基金資助項(xiàng)目（81601153）；江蘇省自然科學(xué)基金資助項(xiàng)目（BK20150104）；南京市醫(yī)學(xué)科技發(fā)展基金資助項(xiàng)目（YKK16083）；南京市科技發(fā)展計(jì)劃項(xiàng)目（201503020）