Acute Administration of Ojeok-san Ameliorates Pain-like Behaviors in Pre-Clinical Models of Inflammatory Bowel Diseases.
Acute Administration of Ojeok-san Ameliorates Pain-like Behaviors in Pre-Clinical Models of Inflammatory Bowel Diseases.
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DOI：
10.3390/nu15071559
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发表时间：
2023-03-23
期刊：
影响因子：
5.9
通讯作者：
Velázquez KT
中科院分区：
文献类型：
--
作者：
Patton EA;Cunningham P;Noneman M;Helms HP;Martinez-Muniz G;Sumal AS;Dhameja MK;Unger CA;Alahdami AK;Enos RT;Chatzistamou I;Velázquez KT
(1)背景：胃肠道疼痛和疲劳是炎症性肠病（IBD）患者最关心的问题。常用处方药的重点是减少过度炎症。然而，高达 20% 处于“不活动”状态的 IBD 患者会出现腹痛。草药 Ojeok-san (OJS) 在改善内脏疼痛方面显示出良好的前景。然而，尚未在 IBD 临床前模型中进行 OJS 的研究。 OJS 促进镇痛的机制仍不清楚，并且尚不清楚 OJS 是否具有成瘾特性。 (2) 目的：在本研究中，我们研究了 OJS 促进镇痛效果和奖励行为的潜力。此外，我们还研究了巨噬细胞中的肿瘤坏死因子 α (TNFα) 是否是 IBD 引起的伤害感受的主要原因。 (3)方法：采用多种IBD动物模型来确定OJS是否可以减轻内脏伤害性感受。使用 TNFα 巨噬细胞缺陷小鼠来研究 OJS 减少伤害性行为的作用机制。机械敏感性和操作条件反射测试用于确定 OJS 的镇痛和奖励作用。评估体重、结肠长度/重量、便血、结肠炎症和全血细胞计数以确定疾病进展。 (4) 结果：OJS 降低了结肠炎葡聚糖硫酸钠模型和 IL-10 敲除（KO）小鼠中诱发的机械性伤害感受，并延迟了 C57BL/6 小鼠对结直肠扩张的厌恶。在 OJS 处理的 IL-10 KO 和 mdr1a KO 小鼠中没有观察到奖励行为。 OJS 的镇痛作用与巨噬细胞 TNFα 水平和 IBD 进展无关。 (5) 结论：OJS 改善可引起机械性和内脏伤害性感受，但不会产生奖励效应。 OJS 的镇痛作用不是由巨噬细胞 TNFα 介导的。
(1) Background: Gastrointestinal pain and fatigue are the most reported concerns of patients with inflammatory bowel disease (IBD). Commonly prescribed drugs focus on decreasing excessive inflammation. However, up to 20% of IBD patients in an “inactive” state experience abdominal pain. The medicinal herb Ojeok-san (OJS) has shown promise in the amelioration of visceral pain. However, no research on OJS has been conducted in preclinical models of IBD. The mechanism by which OJS promotes analgesia is still elusive, and it is unclear if OJS possesses addictive properties. (2) Aims: In this study, we examined the potential of OJS to promote analgesic effects and rewarding behavior. Additionally, we investigated if tumor necrosis factor alpha (TNFα) from macrophages is a primary culprit of IBD-induced nociception. (3) Methods: Multiple animal models of IBD were used to determine if OJS can reduce visceral nociception. TNFα-macrophage deficient mice were used to investigate the mechanism of action by which OJS reduces nociceptive behavior. Mechanical sensitivity and operant conditioning tests were used to determine the analgesic and rewarding effects of OJS. Body weight, colon length/weight, blood in stool, colonic inflammation, and complete blood count were assessed to determine disease progression. (4) Results: OJS reduced the evoked mechanical nociception in the dextran sulphate sodium model of colitis and IL-10 knockout (KO) mice and delayed aversion to colorectal distension in C57BL/6 mice. No rewarding behavior was observed in OJS-treated IL-10 KO and mdr1a KO mice. The analgesic effects of OJS are independent of macrophage TNFα levels and IBD progression. (5) Conclusions: OJS ameliorated elicited mechanical and visceral nociception without producing rewarding effects. The analgesic effects of OJS are not mediated by macrophage TNFα.
影响因子：
5.9
作者：
Han BH;Seo CS;Yoon JJ;Kim HY;Ahn YM;Eun SY;Hong MH;Lee JG;Shin HK;Lee HS;Lee YJ;Kang DG
通讯作者：
Kang DG
影响因子：
2.4
作者：
Gerdjikov TV;Beninger RJ
通讯作者：
Beninger RJ