Nrf2 mediates the antinociceptive activity of dexmedetomidine in an acute inflammatory visceral pain rat model by activating the NF‐κB sensor

Following the publication of the Lan et al. (2020), the author would like to amend the ‘Animal treatment’ section of the Materials and Methods. The authors apologise for the mistake.

The original text read as follows:

2.2 Animal treatment

We randomly divided twenty SD rats into four groups (n=5): normal group (rats given no treatment), model group (treated with acetic acid), vehicle group (subdural administration of 10 mL saline), and DEX group (intrathecal injection of 3 mg DEX). Fifteen minutes after the subdural administration with saline/DEX, acetic acid (3%, 300 mg/kg) was injected into the peritoneal cavity, and the rats were observed for 30 min.12 The pain behaviour was assessed by abdominal withdrawal reflex (AWR), thermal withdrawal latency (TWL), and mechanical withdrawal threshold (MWT). Immediately following the visceral pain experiment, all the rats were sacrificed by administrating sodium pentobarbital (120 mg/kg, IP).

The correct text should read as follows:

2.2 Animal treatment

We randomly divided twenty SD rats into four groups (n=5): normal group (rats given no treatment), model group (treated with acetic acid), vehicle group (intrathecal injection of 20µL saline), and DEX group (intrathecal injection of 2µg,20µLDEX). Fifteen minutes after the intrathecal injection with saline/DEX, acetic acid (3%, 0.1ml) was injected into the peritoneal cavity except for the normal group, and the rats were observed for 30 min.¹² The pain behaviour was assessed by abdominal withdrawal reflex (AWR), thermal withdrawal latency (TWL), and mechanical withdrawal threshold (MWT). Immediately following the visceral pain experiment, all the rats were sacrificed by administrating sodium pentobarbital (120 mg/kg, IP).

REFERENCE

Lan, J, Zheng, J, Feng, J, Peng, W. Nrf2 mediates the antinociceptive activity of dexmedetomidine in an acute inflammatory visceral pain rat model by activating the NF‐κB sensor. Cell Biochem Funct. 2020; 38: 97–105. https://doi.org/10.1002/cbf.3456

Nrf2通过激活NF-κB传感器介导右美托咪定在急性炎症性内脏痛大鼠模型中的镇痛作用

随着兰等人的出版。（2020），作者想修改“材料和方法”中的“动物处理”部分。作者为这个错误表示歉意。

原文内容如下：

2.2动物治疗

我们将20只SD大鼠随机分为四组（n = 5）：正常组（未给予治疗的大鼠），模型组（用乙酸治疗），媒介物组（硬膜下给予10 mL盐水）和DEX组（鞘内注射） 3毫克DEX）。盐水/ DEX硬膜下给药后十五分钟，将乙酸（3％，300 mg / kg）注入腹膜腔，观察大鼠30分钟。12通过腹部撤退反射（AWR）评估疼痛行为），热退缩潜伏期（TWL）和机械退缩阈值（MWT）。内脏疼痛实验后，立即通过给予戊巴比妥钠（120 mg / kg，腹膜内注射）处死所有大鼠。

正确的文本应如下所示：

2.2动物治疗

我们将20只SD大鼠随机分为四组（n = 5）：正常组（未给予治疗的大鼠），模型组（用乙酸处理），媒介物组（鞘内注射20µL盐水）和DEX组（鞘内注射2µg，20µLDEX）。鞘内注射生理盐水/ DEX 15分钟后，除正常组外，向腹膜腔注射乙酸（3％，0.1ml），观察大鼠30分钟。¹²通过腹部退缩反射（AWR），热退缩潜伏期（TWL）和机械退缩阈值（MWT）评估疼痛行为。内脏疼痛实验后，立即通过给予戊巴比妥钠（120 mg / kg，腹膜内注射）处死所有大鼠。

参考

Lan，J，Zheng，J，Feng，J，Peng，W.Nrf2通过激活NF-κB传感器介导右美托咪定在急性炎症性内脏痛大鼠模型中的镇痛作用。细胞生化功能。2020年；38：97-105。https://doi.org/10.1002/cbf.3456