FIGURE 7
Continuous injection of cyclotraxin-B into the insular cortex reduced
chronic corneal pain induced corneal hypersensitivity and inhibited
descending inflammatory factor upregulation. (a) Diagram and timeline
schema of the experimental design. Grey arrows mark local infusion of
cyclotraxin-B or saline into the insular cortex. Bilateral extraorbital
glands were excised on day 0. Insular cortex cannula was inserted on day
21 after surgery. Dark grey circles mark behavior test including
chemical and mechanical corneal sensitivity test. Black circles mark
open field test. Light grey circles mark tissue sampling with qRT-PCR.
(b-e) The protein expression of TNFα, IL-6, IL-10 and IL-1β in DE mice
after consecutive administration of cyclotraxin-B
(10 µg/µL, 0.05 µL per side for five days) (n=4, *P < 0.05 and
**P < 0.01 versus DE group). (f-l) Effect of treatment with
BDNF antagonist cyclotraxin-B induces a statistically significant
antinociceptive effect in chemical and mechanical corneal sensitivity,
whereas during anxiolytic effect is unremarkable. The DE+Cyclotraxin-B
group represents that of dry eye mice receiving an intra-insular
cortical microinjection of cyclotraxin-B (10 µg/µL, 0.05 µL per side;
MCE). (f-i) The chemical and mechanical thresholds after administration
of cyclotraxin-B in DE mice (n=8, **P < 0.01, ***P <
0.001 and ****p < 0.0001 versus DE+Saline group). (j-l) j
Representative activity tracking OFT in Sham, DE, DE+ Cyclotraxin-B,
DE+Saline mice. k,l Time in center region (k) and total distance
traveled (l) during OFT. (n = 6, ****p < 0.0001 versus Sham
group). DE, dry eye; CTB, cyclotraxin-B; QPCR, quantitative polymerase
chain reaction; NS, normal saline; ns, not significant; TNFα, tumor
necrosis factor α; IL-6, Interleukin-6; IL-10, Interleukin-10; IL-1β,
Interleukin-1β. OFT, open field test.