A Study on THE Mechanism of Electroacupuncture to Alleviate Visceral Pain and NGF Expression.

Visceral pain is unbearable, and natural methods are needed to relieve it. Electroacupuncture is a relatively new technique that helps relieve visceral pain by improving blood circulation and providing energy to clogged parts of the body. However, its analgesic effect and mechanism in colorectal pain are still unknown. In this study, the visceral pain models of electroacupuncture in rats were compared and discussed, using nanocomponents to stimulate the expression and mechanism of the nerve growth factor in colorectal pain and electroacupuncture and to observe the expression and mechanism of nerve growth factor in visceral pain relief rats induced by nanocomponents and electroacupuncture. The results show that nanocomponents can effectively relieve visceral pain under the action of electroacupuncture. NGF can activate endogenous proliferation, migration, differentiation, and integration. NSC can promote nerve regeneration and recovery after injury.

The Effect of Transcutaneous Electrical Acupoint Stimulation on Postoperative Catheter-Related Bladder Discomfort in Patients Undergoing Transurethral Resection of the Prostate.

BACKGROUND: Catheter-related bladder discomfort (CRBD), an extremely distressing complication secondary to an indwelling urinary catheterization, is frequently reported in patients with transurethral resection of the prostate (TURP), postoperatively. A prospective, randomized, controlled, double-blind study was designed to assess the efficacy of transcutaneous electrical acupoint stimulation (TEAS) as a treatment for CRBD in patients undergoing TURP. METHODS: Seventy benign prostatic hyperplasia male patients undergoing TURP under general anesthesia requiring intraoperative urinary catheterization were enrolled for the trial. An experienced acupuncturist performed TEAS for 30 minutes before general anesthesia with acupoints RN7, RN6, RN5, RN4, and RN3 and bilateral BL32, BL33, and BL34. Mean arterial pressure (MAP), heart rate (HR), oxygen saturation (SPO2), body temperature (T), and blood samples were collected during the surgery. A series of assessments included the incidence and severity of CRBD, postoperative pain, nausea and vomiting, and physical and mental state measurements. RESULTS: The incidence of CRBD was significantly lower in TEAS group than in control group at the time T5 [9(26%) vs. 28(80%), P < 0.001], T9 [20(57%) vs. 28(80%), P=0.039], T11 [7(20%) vs. 31(89%), P < 0.001], and T12 [4(11%) vs. 7(20%), P=0.003]. The severity of CRBD was significantly lower in TEAS group than in control group at the time T5 [0 vs. 10 (29%), P < 0.001], T9 [2(6%) vs. 10(29%), P=0.011], and T11 [0 vs .9(26%), P=0.002]. The QoR-40 total score was higher in TEAS group at time T11 [191.7(4.4) vs. 189.1(4.3), P=0.007] and T12 [195.3(1.9) vs. 193.3(3.0), P < 0.001]. The postoperative analgesia requirement was higher in control group [5.0(2.9) vs. 3.8(1.9), P=0.045]. CONCLUSIONS: TEAS could significantly prevent the incidence and severity of CRBD, reduce the postoperative analgesic requirement in the early postoperative period, and promote the quality of early recovery in patients undergoing TURP.

Role of Wnt/ß-catenin in the tolerance to focal cerebral ischemia induced by electroacupuncture pretreatment.

Previous studies have demonstrated that pretreatment with electroacupuncture (EA) elicits rapid tolerance to focal cerebral ischemia and that Wnt/ß-catenin plays an essential role in cell survival and proliferation. In the present study, we investigated the role of Wnt/ß-catenin in EA pretreatment-induced neuroprotection. Two hours after EA pretreatment, focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 2 h. Neuronal survival, cell apoptosis, and the Garcia neurological deficit scores were evaluated 24 h after reperfusion. Moreover, learning and memory deficits were assessed 24 h after reperfusion using the Morris water maze test. Finally, the expression of ß-catenin and the B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax) ratio were investigated in the presence and absence of the Wnt/ß-catenin antagonist Dickkopf-1 (Dkk-1), which was administered 30 min before MCAO. We observed that EA pretreatment significantly increased the neuronal expression of ß-catenin in the hippocampus 24 h after reperfusion. Moreover, EA pretreatment improved the neurological outcomes, decreased neuronal loss, inhibited apoptosis, and reversed learning and memory deficits following reperfusion. These beneficial effects of EA were attenuated by Dkk-1, which effectively reversed the expression of ß-catenin. Furthermore, the administration of a Wnt/ß-catenin agonist upregulated the expression of ß-catenin and the Bcl-2/Bax ratio. These results suggest that Wnt/ß-catenin plays a role in the protective effects of EA pretreatment against cerebral ischemia, thus providing evidence of a novel mechanism underlying EA-pretreatment-induced rapid tolerance to focal cerebral ischemia.

[Effect of ginsenoside Rb1 on cerebral infarction volume and IL-1 beta in the brain tissue and sera of focal cerebral ischemia/reperfusion injury model rats].

OBJECTIVE: To investigate the effect of ginsenoside Rb1 on cerebral infarction volume as well as IL-1 beta in the brain tissue and sera of focal cerebral ischemia/reperfusion (I/R) injury model rats. METHODS: The I/R rat model was established by using thread according to Zea-Longa. SD rats were randomly divided into five groups, i.e., the sham-operation group, the model group, the low dose ginsenoside Rb1 (20 mg/kg) group, the medium dose ginsenoside Rb1 group (40 mg/kg), and the high dose ginsenoside Rb1 group (80 mg/kg), 12 in each group. Rats in the sham-operation group only received middle cerebral artery occlusion (MCAO) but without thread insertion. The MCAO model was prepared in the rest 4 groups, followed by MCAO2 h later. Ginsenoside Rb1 at each dose was peritoneally administrated to rats in corresponding groups immediately after cerebral ischemia. Equal volume of normal saline was administered to rats in the sham-operation group. Rats' cerebral infarction volume, integrals of neurologic defect degree, expression of IL-1 beta content in the brain tissue and sera were observed 24 h after 2-h cerebral I/R. RESULTS: In the model group, integrals of neurologic defect degree were improved (P < 0.01), IL-1 beta positive cells in the brain tissue increased and serum IL-1 beta content elevated (P < 0.05), when compared with the sham-operation group. In comparison of the model group, integrals of neurologic defect degree were lowered in the medium dose and high dose ginsenoside Rb1 groups (P < 0.05, P < 0.01). The cerebral infarction volume was all shrunken in each ginsenoside Rb1 group, IL-1 beta positive cells in the brain tissue decreased, and IL-1 beta content in serum reduced (P < 0.01, P < 0.05). Compared with the low dose ginsenoside Rb1 group, integrals of neurologic defect degree decreased, the cerebral infarction volume shrunken, and IL-1 beta content in serum reduced in the high dose ginsenoside Rb1 group (P < 0.01, P < 0.05). CONCLUSION: Ginsenoside Rb1 (20, 40, 80 mg/kg) might effectively release local cerebral ischemia by down-regulating the IL-1 beta expression.