Clindamycin, a bacteriostatic semisynthetic lincosamide, is useful in the management of infections caused by aerobic and anaerobic Gram-positive cocci, including bacteremic pneumonia, streptococcal toxic shock syndrome and sepsis. It has been recently demonstrated that clindamycin inhibits in vitro and in vivo inflammatory cytokine production. In the present study, we investigated the effects of clindamycin in acute and chronic models of pain and inflammation in mice and the underlying mechanisms. Intraperitoneal (i.p.) administration of clindamycin (400 mg/kg) increased the animal’s latency to exhibit the nociceptive behavior induced by noxious heat (hot plate model). Intrathecal injection of clindamycin (2, 10 and 50 µg) also increased the animals’ latency to exhibit the nociceptive behavior. Tactile hypersensitivity and paw edema induced by intraplantar (i.pl.) injection of carrageenan were attenuated by previous administration of clindamycin (200 and 400 mg/kg, i.p.). Clindamycin (100, 200 and 400 mg/kg, i.p.) also attenuated ongoing tactile hypersensitivity and paw edema induced by i.pl. injection of complete Freund’s adjuvant (CFA). The antinociceptive activity of clindamycin (400 mg/kg, i.p.) in the hot plate model was attenuated by previous administration of naltrexone (5 and 10 mg/kg, i.p.), but not glibenclamide or AM251. CFA-induced production of TNF-α and CXCL-1 was reduced by clindamycin (400 mg/kg, i.p.). Concluding, clindamycin exhibits activities in acute and chronic models of pain and inflammation. These effects are associated with reduced production of TNF-α and CXCL-1 and activation of opioidergic mechanisms. Altogether, these results indicate that the clindamycin’s immunomodulatory effects may contribute to a pharmacological potential beyond its antibiotic property.

中文翻译：

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克林霉素可通过减少肿瘤坏死因子-α和CXCL-1的产生并激活视皮醇功能来抑制伤害感受。

克林霉素是一种具有抑菌作用的半合成林可酰胺，可用于控制由需氧和厌氧的革兰氏阳性球菌引起的感染，包括细菌性肺炎，链球菌中毒性休克综合征和败血症。最近已经证明克林霉素抑制体外和体内炎性细胞因子的产生。在本研究中，我们研究了克林霉素在小鼠疼痛和炎症的急性和慢性模型中的作用及其潜在机制。克林霉素（400 mg / kg）的腹膜内（ip）给药增加了动物的潜伏期，表现出有毒热诱导的伤害性行为（热板模型）。鞘内注射克林霉素（2、10和50 µg）也增加了动物表现出伤害性行为的潜伏期。预先给予克林霉素（200和400 mg / kg，腹腔注射）可减轻足底内（i.pl.）注射角叉菜胶引起的触觉超敏反应和爪水肿。克林霉素（100、200和400 mg / kg，腹腔注射）也减弱了i.pl引起的持续的触觉超敏反应和爪水肿。注射完全弗氏佐剂（CFA）。先前服用纳曲酮（5和10 mg / kg，腹腔注射）可减轻克林霉素（400 mg / kg，腹腔注射）在热板模型中的镇痛作用，但不给予格列本脲或AM251。克林霉素（400 mg / kg，腹膜内）可降低CFA诱导的TNF-α和CXCL-1的产生。最后，克林霉素在急性和慢性疼痛和炎症模型中均具有活性。这些作用与减少的TNF-α和CXCL-1的产生以及阿片肌功能机制的激活有关。