[Electroacupuncture improves long-term survival of myocardial infarction mice by promoting myocardial angiogenesis and inhibiting ventricular remodeling].

OBJECTIVE: To investigate the mechanism of electroacupuncture (EA) in improving the long-term survival rate of mice after myocardial infarction by promoting angiogenesis and inhibiting ventricular remodeling. METHODS: A total of 102 male C57BL/6 mice were randomly divided into sham operation, model and EA groups (n=34 /group). The myocardial infarction model was established by permanent ligation of the anterior descending branch of the left coronary artery. Beginning from the 3rd day after ligation, EA (2 Hz/20 Hz) was applied to bilateral "Neiguan" (PC6) and "Ximen" (PC4) for 30 min, once a day for 28 days. The survival rate in 140 d was recorded and the left ventricular ejection fraction (EF) calculated by using echocardiography after the treatment. The left cardiac ventricular tissue was cut into sections to be stained with Masson's trichrome, wheat germ agglutinin (WGA) or α-smooth muscle actin (α-SMA) immunohistochemistry method, followed by measuring the collagen area in the marginal region of myocardial infarction and calculating the collagen volume fraction (for assessing the severity of myocardial fibrosis), measuring the sectional area of cardiomyocytes (for assessing the degree of myocardial hypertrophy), and ob-serving the newborn blood vessels and calculating the ratio of neovascularization area (for assessing the state of angiogenesis). The expression of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor (HIF)-1α protein in the boundary area of myocardial infarction were detected by Western blot. RESULTS: After modeling, the survival rate, EF, and the thickness of the left cardiac ventricle were significantly decreased (P<0.01), whereas the percentage of collagen deposition area, sectional area of cardiomyocyte, percentage of angiogenesis area, and the expression levels of VEGF and HIF-1α proteins were significantly increased (P<0.01) in the model group relevant to the sham operation group. Compared with the model group, the survival rate, EF, the thickness of the left cardiac ventricle, the percentage of angiogenesis area, and the expression levels of VEGF and HIF-1α proteins were significantly increased (P<0.05, P<0.01), while the percentage of collagen deposition area and the sectional area of the cardiomyocyte were considerably decreased in the EA group (P<0.01, P<0.05). CONCLUSION: EA of PC6 and PC4 can significantly improve the cardiac function and long-term survival rate in mice with myocardial infarction, which may be related to its functions in up-regulating the expression of HIF-1α and VEGF to promote angiogenesis and in inhibiting ventricular remodeling.

Electroacupuncture treatment ameliorated the long-term cognitive impairment via activating eNOS/NO pathway and related Aß downregulation in sepsis-survivor mice.

OBJECTIVE: Sepsis is a major challenge in intensive care unit worldwide and the septic survivors are left with long-term cognitive deficits. This work aims to explore the effects of electroacupuncture (EA) on long-term cognitive function and its underlying mechanism in sepsis-survivor mice. METHODS: Sepsis was induced by cecal ligation and puncture in C57BL/6 male mice. Seven days post-surgery, sepsis-survivor mice were treated with EA or nonacupoint EA for 17 days twice daily. Then, cognitive function was evaluated by Morris water maze task. The hippocampus tissue were collected from the mice at 30 days post-surgery. The level of nitric oxide and the expression of endothelial nitric oxide (eNOS), phospho-eNOS (p-eNOS), and amyloid ß-peptide (Aß) were measured. RESULTS: Compared with the sham-operated control, sepsis-survivors had significant cognitive deficits evidenced by the increased time of escape latency and reduced crossing number in Morris water maze task, as well as lower NO and p-eNOS level and higher Aß level. EA treatment at GV20 and ST36 acupoints but not at a nonacupoint improved the cognitive function, increased the NO and p-eNOS level, and decreased Aß generation; while eNOS inhibitor (l-NAME) undermined the efficacy of EA treatment. CONCLUSION: In conclusion, repeated EA treatment could ameliorate the long-term cognitive impairment via manipulating the expression of p-eNOS and related Aß in sepsis-survivor mice.

Electroacupuncture ameliorates postoperative cognitive dysfunction and associated neuroinflammation via NLRP3 signal inhibition in aged mice.

BACKGROUND: Postoperative cognitive dysfunction (POCD) is associated with worsened prognosis especially in aged population. Clinical and animal studies suggested that electroacupuncture (EA) could improve POCD. However, the underlying mechanisms especially EA's regulatory role of inflammasomes remain unclear. METHODS: The model of POCD was established by partial hepatectomy surgery in 18-month mice with or without postoperative EA treatment to the Baihui acupoint (GV20) for 7 days. Cognitive functions were assessed by Morris water maze test, and proinflammatory cytokines IL-1ß and IL-6 and microglia activity were assayed by qPCR, ELISA, or immunohistochemistry. Tight junction proteins, NLRP3 inflammasome and downstream proteins, and NF-κB pathway proteins were evaluated by western blotting. RESULTS: EA markedly preserved cognitive dysfunctions in POCD mice, associated with the inhibition of neuroinflammation as evidenced by reduced microglial activation and decreased IL-1ß and IL-6 levels in brain tissue. EA also preserved hippocampal neurons and tight junction proteins ZO-1 and claudin 5. Mechanistically, the activation of NLRP3 inflammasome and NF-κB was inhibited by EA, while NLRP3 activation abolished EA's treatment effects on cognitive function. CONCLUSION: EA alleviates POCD-mediated cognitive dysfunction associated with ameliorated neuroinflammation. Mechanistically, EA's treatment effects are dependent on NLRP3 inhibition.