Shu-Mei Chen1, Mao-Hsien Wang2, Hung-Sheng Soung3, Hsiang-Chien Tseng4, Chih-Hsiang Fang5, Yi-Wen Lin6, Chih-Chuan Yang7, Cheng-Chia Tsai8. 1. Department of Neurosurgery, Taipei Medical University Hospital, Taipei Medical University, Taipei, 110, Taiwan, ROC; Department of Surgery, School of Medicine, Taipei Medical University, Taipei, 110, Taiwan, ROC. 2. Department of Anesthesia, En Chu Kon Hospital, Sanshia District, New Taipei City, 23702, Taiwan, ROC. 3. Department of Psychiatry, Yuan-Shan Br. of Taipei Veteran General Hospital, Yilan County, 26604, Taiwan, ROC; Department of Biomedical Engineering, National Defense Medical Center, Taipei, 11490, Taiwan, ROC. 4. Department of Anesthesiology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, 11101, Taiwan, ROC; School of Medicine, Fu Jen Catholic University, New Taipei City, 24205, Taiwan, ROC. 5. China Medical University Hospital, Taichung City, 404332, Taiwan, ROC; Trauma and Emergency Center, China Medical University Hospital, Taichung City, 404018, Taiwan, ROC. 6. Institute of Biomedical Engineering, National Taiwan University, Taipei, 10051, Taiwan, ROC. 7. Department of Neurosurgery, Mackay Memorial Hospital, Taipei, 10449, Taiwan, ROC; Department of Nursing, Mackay Junior College of Medicine, Nursing and Management, Taipei, 11260, Taiwan, ROC. 8. Department of Neurosurgery, Mackay Memorial Hospital, Taipei, 10449, Taiwan, ROC; Department of Medicine, Mackay Medical College, New Taipei City, 252, Taiwan, ROC. Electronic address: dschang580704@yahoo.com.tw.
Abstract
BACKGROUND/ PURPOSE: We investigated the protective efficacy of l-theanine (LT), the major amino acid components of green tea, on chronic constriction injury (CCI) of sciatic nerve-induced neuropathic pain (NP) development and neuronal functional changes in rats. METHODS: Rats with NP induced by CCI of the left sciatic nerve and sham-operated rats received LT or saline solution, with pain sensitive tests of thermal hyperalgesia and mechanical allodynia. Motor and sensory nerve conduction velocities were measured after surgery. Subsequently, the rats were sacrificed; the sciatic nerve was excised, homogenized, prepared and subjected for estimation of nitric oxide (NO), malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), myeloperoxidase (MPO), and caspase-3. RESULTS: CCI produced a significant increase in hyperalgesia and allodynia, an increase in SFI, a decrease in nerve conduction velocity, increases in NO, MDA, TNF-α, IL-1β, IL-6, MPO, and caspase-3 levels, as well as reduction of GSH, SOD, and CAT in the rat sciatic nerve. LT treatment significantly and dose-dependently alleviated CCI-induced nociceptive pain thresholds and ameliorated abnormal nerve conduction and functional loss in rats with CCI. Moreover, LT treatment reduced NO and MDA levels, increased antioxidative strength, and markedly suppressed the levels of neuroinflammatory and apoptotic markers in injured sciatic nerves. CONCLUSION: This is the first report on the ameliorative effect of LT in CCI-induced NP in rats. This effect might be attributed to its anti-oxidative, anti-inflammatory, anti-apoptotic, and neuroprotective, thus making it potentially useful as an adjuvant to conventional treatment.
BACKGROUND/ PURPOSE: We investigated the protective efficacy of l-theanine (LT), the major amino acid components of green tea, on chronic constriction injury (CCI) of sciatic nerve-induced neuropathic pain (NP) development and neuronal functional changes in rats. METHODS: Rats with NP induced by CCI of the left sciatic nerve and sham-operated rats received LT or saline solution, with pain sensitive tests of thermal hyperalgesia and mechanical allodynia. Motor and sensory nerve conduction velocities were measured after surgery. Subsequently, the rats were sacrificed; the sciatic nerve was excised, homogenized, prepared and subjected for estimation of nitric oxide (NO), malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), myeloperoxidase (MPO), and caspase-3. RESULTS: CCI produced a significant increase in hyperalgesia and allodynia, an increase in SFI, a decrease in nerve conduction velocity, increases in NO, MDA, TNF-α, IL-1β, IL-6, MPO, and caspase-3 levels, as well as reduction of GSH, SOD, and CAT in the rat sciatic nerve. LT treatment significantly and dose-dependently alleviated CCI-induced nociceptive pain thresholds and ameliorated abnormal nerve conduction and functional loss in rats with CCI. Moreover, LT treatment reduced NO and MDA levels, increased antioxidative strength, and markedly suppressed the levels of neuroinflammatory and apoptotic markers in injured sciatic nerves. CONCLUSION: This is the first report on the ameliorative effect of LT in CCI-induced NP in rats. This effect might be attributed to its anti-oxidative, anti-inflammatory, anti-apoptotic, and neuroprotective, thus making it potentially useful as an adjuvant to conventional treatment.