ABSTRACT
Objective To evaluate the effect of electroacupuncture ( EA) preconditioning on hipp-ocampal I-kappa B-α ( IκB-α)∕nuclear factor κB ( NF-κB)∕intercellular adhesion molecule-1 ( ICAM-1) signaling pathway during cerebral ischemia-reperfusion ( I∕R) in mice. Methods A total of 120 healthy male C57BL∕6 mice, aged 10-12 weeks, weighing 20-25 g, were divided into 4 groups ( n=30 each) u-sing a random number table method: control group ( group C) , cerebral I∕R group ( group I∕R) , precondi-tioning with EA at non-acupoint+cerebral I∕R group ( group S+I∕R) and preconditioning with EA at Baihui acupoint + cerebral I∕R group ( group E+I∕R) . The cerebral I∕R injury model was established by occlusion of bilateral common carotid arteries followed by reperfusion for 72 h in mice anesthetized with halothane or chloral hydrate in group I∕R. Group S+I∕R received EA at the points 2 mm lateral to the acupoints of Baihui for 5 consecutive days, and then the cerebral I∕R injury model was established. Group E+I∕R received EA at Baihui acupoints with a sparse-dense wave at an intensity of 1 mA and a frequency of 2 Hz∕15 Hz for 30 min once a day for 5 consecutive days, and then the cerebral I∕R injury model was established. Neurobe-havioral score was assessed at 24 and 48 h of reperfusion. Then 5 mice in each group were sacrificed, and the hippocampal tissues were obtained and stained with haematoxylin and eosin for examination of the patho-logical changes in hippocampal CA1 region and for determination of the expression of IκB-α, NF-κB, ICAM-1, interleukin-6 ( IL-6) , IL-1β protein and mRNA by Western blot and real-time polymerase chain reaction, respectively. Results Compared with group C, neurobehavioral score was significantly in-creased, and the expression of hippocampal IκB-α, NF-κB, ICAM-1, IL-6 and IL-1βprotein and mRNA was up-regulated in I∕R, S+I∕R and E+I∕R groups ( P<0. 05) . Compared with group I∕R, neurobehavioral score was significantly decreased, and the expression of hippocampal IκB-α, NF-κB, ICAM-1, IL-6 and IL-1β protein and mRNA was down-regulated in group E+I∕R (P<0. 05), and no significant change was found in the parameters mentioned above in group S+I∕R (P>0. 05). Compared with group S+I∕R, neu-robehavioral score was significantly decreased, and the expression of hippocampal IκB-α, NF-κB, ICAM-1, IL-6 and IL-1β protein and mRNA was down-regulated in group E+I∕R ( P<0. 05) . Conclusion The mechanism by which EA preconditioning attenuates cerebral I∕R injury may be related to inhibiting activation of hippocampal IκB-α∕NF-κB∕ICAM-1 signaling pathway in mice.
ABSTRACT
Objective To explore the roles of IκBα and TGF-β1 on airway inflammation in rats with chronic bronchitis induced by smoking and study the effects and mechanism of anti-inflammation of pretreatment with ambroxol. Methods Sixty male wistar rats were randomly divided into four groups: Normal dosage group, model group, high dosage group and low dosage group. The rats with chronic bronchitis were established by smoking. For high and low dosage group, rats were pretreated respectively with ambroxol group, rats were pretreated with normal saline through peritoneal injection as much as the low dosage group.After 76 days, the histopathologic changes stained in hemotoxylin and eosin (H. E.) of bronchopulmonary tissues were observed under opticalmicroscope, white cell counts and differential analysis were performed in BALF, the expression of IκBα and TGF-β1 were detected by immunohistochemistry. Results The pathological changes of model group were in consistent with that of chronic bronchitis, but the degrees were significantly reduced in high and low dosage groups. Compared with those in normal group, the white cell count and the neutrophilic granulocyte count of BALF in model group were significantly increased and the macrophagocyte count decreased, and the expression of IκBαwas significantly decreased(t =3.24,3.31,3.29,3.48, P ＜0. 05) and the TGF-β1 significantly increased (P ＜0. 05). Compared with those in the model group, the white cell count and the neutrophilic granulocyte count of BALF in high and low dosage group were significantly decreased and the macrophagocyte count increased, the expression of IκBαwas significantly increased (t =2. 86,2. 97,2. 92,3.52,2.42,2. 88,2. 58,3.48, P ＜0. 05) and the TGF-β1 significantly decreased (P ＜0. 05) . Compared with those in low dosage group, the expression of TGF-β1 was decreased and the expression of IκBαincreased in high dosage group (t =2. 82,3.64, P ＜0. 05). Conclusions Down-regulating the expression of IκBα and up-regulating of TGF-β1 may be involved in the process of airway inflammation in rats with chronic bronchitis induced by smoking. Ambroxol might have better effects on ameliorating airway inflammation by up-regulating the expression of IκBα and down-regulating of TGF-β1.