BACKGROUND: Up to now, few studies related to the mechanism of low-frequency transcutaneous electrical nerve stimulation (TENS) in relieving pain, and the effect of low-frequency TENS on the activity potential of dorsal horn cells in rats after peripheral nerve injury. OBJECTIVE: To observe the effects of low-frequency TENS on the activity potential of dorsal horn cells induced by mechanical allodynia and thermal allodynia by using animal models of peripheral nerve injury, and observe the efficacy after interfering of naloxone. DESIGN: A randomized control animal study. SETTING: Department of Neurology, Affiliated Hospital of Medical College, Yanbian University. MATERIALS: The experiment was carried out in the central laboratory of Medical College, Yanbian University between February and October 2004. Eighty male Sprague-Dawley rats were used, and 60 random selected ones were operated to separate sciatic nerve, two branch tibial nerves and sural nerves of sciatic nerve were amputated after ligation, and peroneal nerve was left as the experimental group; the other 20 rats were placed at the origin after sciatic nerve was separated, and then the skin was sutured as the control group. METHODS: ① Pain detection (Behavioral test): At 1 week postoperatively, the rats were given mechanical allodynia and thermal allodynia once every 5 seconds for 10 times, and then the frequency of foot withdrawal was detected (0%-40% for mild pain, 40%-70% for moderate pain; 70% and above for severe pain). ② The spontaneous activity potential of dorsal horn cells and that induced by mechanical allodynia and thermal allodynia were detected among the rats with moderate and severe pain in the control group and study group. ③ Low-frequency TENS of 3 mA and 10 Hz was applied to the legs of rats in the experimental group with annular electrode for 10 minute, and the membrane potential of dorsal horn cell was detected before and after stimulation. ④ At the same time of low-frequency TENS was given, rats in the experimental group were injected with naloxone via audal vein, and the membrane potential of dorsal horn cell was detected before and at 10 minutes after naloxone injection.RESULTS: Finally 80 rats were involved in the analysis of results after compensation. ① The foot withdrawal frequencies induced by mechanical allodynia and thermal allodynia in the experimental group were obviously higher than those in the control group (P ＜ 0.01). ② The membrane potential of dorsal horn cell by mechanical allodynia and thermal allodynia in the experimental group were obviously higher than those in the control group (P ＜ 0.01). ③ The membrane potential of dorsal horn cell by mechanical allodynia and thermal allodynia at 10 minutes after low-frequency TENS in the experimental group were obviously higher than those in the control group [(102.6±0.9), (136.9±1.46) impulses per 10 seconds; (175.2±1.28), (240.8±1.51) impulses per 10 seconds, P ＜ 0.01]. ④ In the experimental group, the membrane potential of dorsal horn cell by mechanical allodynia and thermal allodynia at 10 minutes after naloxone injection were obviously higher than those before injection [(174.5±0.4), (235.4±1.4) impulses per 10 seconds, P ＜ 0.01].CONCLUSION: Low-frequency TENS can effectively inhibit the activity potential of spinal dorsal horn cells induced by non-noxious stimulation,and the intravenous injection of naloxone (8 mg/kg) can recover it to the pretreatment level, indicating that low-frequency TENS may alleviate pain by stimulating central nervous system to make it secrete endogenous opium system, and acting on spinal dorsal horn cells to reduce the activity.

The liver injury induced by Polygonum multiflorum Thunb. (PM) was investigated based on idiosyncratic hepatotoxicity model co-treated with lipopolysaccharide (LPS) at a non-hepatotoxic dose. Sprague-Dawley (SD) rats were intragastrically administered with three doses (18.9, 37.8, 75.6 g crude drug per kg body weight) of 50% alcohol extracts of PM alone or co-treated with non-toxic dose of LPS (2.8 mg·kg(-1)) via tail vein injection. The plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were assayed and the isolated livers were evaluated for histopathological changes. The dose-toxicity relationships of single treatment of PM or co-treatment of LPS were investigated comparatively to elucidate the idiosyncratic hepatotoxicity of PM. The results showed that no significant alterations of plasma ALT and AST activities were observed in the groups of solo-administration of LPS (2.8 mg·kg(-1), i.v.) or different dosage (18.9, 37.8 and 75.6 g·kg(-1), i.g.) of PM, compared to normal control group (P > 0.05); while significant elevations were observed in the co-administration groups of PM and LPS. Treatment with LPS alone caused slight infiltration of inflammatory cells in portal area but no evident hepatocytes injury. Co-treatment with LPS and PM (75.6 g·kg(-1), i.g.) caused hepatocyte focal necrosis, loss of central vein intima and a large number of inflammatory cell infiltration in portal areas. When further reduce the dosage of PM, significant increases of plasma ALT and AST activities (P < 0.05) were still observed in co-administration groups of LPS and PM (1.08 or 2.16 g·kg(-1)), but not in LPS or PM solo-administration groups. Nevertheless, the co-treatment of low dosage of PM (0.54 g·kg(-1)) with LPS did not induce any alteration of plasma ALT and AST. In conclusion, intragastric administration with 75.6 g·kg(-1) of PM did not induce liver injury in normal rats model; while the 2 folds of clinical equivalent dose of PM (1.08 g·kg(-1)) could result in liver injury in the LPS-based idiosyncratic hepatotoxicity model, which could be used to evaluate the idiosyncratic hepatotoxicity of PM.