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Published on: July 16, 2014
Minocycline attenuates pain by inhibiting spinal microglia activation in diabetic rats
Jin-Shan Sun1, Yu-Jie Yang2, Yong-Zhen Zhang1
1Department of Gastroenterology, Changhai Hospital, The Second Military Medical University, Shanghai 200433, P.R. China.
Abstract:
The mechanisms associated with diabetes-induced neuropathic pain are complex and poorly understood. In order to understand the involvement of spinal microglia activity in diabetic pain, the present study investigated whether minocycline treatment is able to attenuate diabetic pain using a rat model. Diabetes was induced using a single intraperitoneal injection of streptozotocin (STZ). Minocycline was then intrathecally administered to the rats. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were tested weekly. The expression of OX-42, Iba-1, phospho-p38 mitogen-activated protein kinase (MAPK), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and inducible nitric oxide synthase (iNOS), were examined in the spinal cord in order to evaluate the activation of microglia. The present study demonstrated that rats with STZ-induced diabetes exhibited increased mean plasma glucose concentration, decreased mean body weight and significant pain hypersensitivity compared with control rats. PWT and PWL values of rats with STZ-induced diabetes increased following treatment with minocycline. No differences were observed in expression levels of the microglial activity markers (OX-42, Iba-1 and phospho-p38 MAPK) between rats with STZ-induced diabetes and control rats. However, TNF-α, IL-1β and iNOS expression levels were higher in rats with STZ-induced diabetes compared with control rats. Following treatment with minocycline markers of microglial activation, including cytokines and iNOS, were downregulated in rats with STZ-induced diabetes. The results of the present study indicated that minocycline treatment may inhibit spinal microglial activation and attenuate diabetic pain in rats with STZ-induced diabetes.
Insights
Minocycline treatment reduced pain hypersensitivity in rats with diabetes by inhibiting spinal microglia activation and downregulating inflammatory markers like TNF-α and IL-1β.
Area of Science:
- Neuroscience
- Pharmacology
- Endocrinology
Background:
- Diabetic neuropathic pain mechanisms are complex and not fully understood.
- Spinal microglia activation is implicated in the development of diabetic pain.
Purpose of the Study:
- To investigate if minocycline can attenuate diabetic pain.
- To explore the role of spinal microglia in STZ-induced diabetic pain.
Main Methods:
- Diabetes was induced in rats using streptozotocin (STZ).
- Minocycline was administered intrathecally.
- Pain behaviors (PWT, PWL) were assessed.
- Spinal cord expression of microglial markers (OX-42, Iba-1, phospho-p38 MAPK) and inflammatory mediators (TNF-α, IL-1β, iNOS) were analyzed.
Main Results:
- STZ-induced diabetic rats showed pain hypersensitivity, elevated glucose, and reduced body weight.
- Minocycline treatment improved PWT and PWL in diabetic rats.
- While OX-42, Iba-1, and phospho-p38 MAPK levels were unchanged, TNF-α, IL-1β, and iNOS were elevated in diabetic rats and reduced by minocycline.
Conclusions:
- Minocycline treatment attenuates diabetic pain in rats.
- Minocycline may exert its effects by inhibiting spinal microglial activation and reducing pro-inflammatory cytokine and iNOS expression.
