| Large number of experimental and clinical study found that stress can cause changes in immune function. Surgery as a means of clinical treatment, inevitably cause trauma and affect the immune system. Traumatic stress can cause suppression of immune function and even cause immune deficiency. The longer immunosuppression duration, the more complicated the chance of infection, serious or even life-threatening. How to improve immune function, enhanced disease resistance is an issue of general interest.The long-term clinical practice test has confirmed that acupuncture is really effective for some diseases. Acupuncture is not directly on the pathogenic factors, but one way is to stability by rebuilding the immune system. Large number of clinical and basic research confirmed that acupuncture has effect on the body's immune system regulation. Chinese medicine treatment can be used to treat deficiency of the method of immunosuppressive diseases. Acupuncture can improve the body's immune function. Previous studies in our laboratory also show that acupuncture therapy can improve post-traumatic stress immunosuppressed rats. This work from acupuncture research, discusses bilateral electroacupuncture (EA) "Zusanli" Points on immunity of rats with traumatic stress.Extracellular signal-regulated kinase (ERK), is related to a variety of stress. ERK1/ 2 are closely related to brain injury and inflammation. ERK5 MAPK signaling pathway is relatively new and it can be activated by various stimuli, including mitogen (such as EGF) and some cell stress and so on. Our work have showed that phosphorylation of ERK1/2 in the cerebral cortex of rats after trauma could change, and it suggested that ERK1/2 might be involved in immunosuppressed in rats of trauma.It is reported that upstream kinase MEK5 of ERK5 is highly expressed in the brain, and immune organs (thymus, spleen) in adult mice. So we propose that expression of the phosphorylation of ERK5 could be changed after trauma? Is ERK5 involved in immune suppression in traumatic rats? First, the changes of the expression of phosphorylated ERK1/2 and of phosphorylated ERK5 after trauma in rats and the impact by electrical acupunctureAfter 24 h of trauma in rats, the expression of phosphorylated ERK1/2 and of phosphorylated ERK5 is increased in the cerebral cortex by immunohistochemistry. The expression of phosphorylated ERK1/2 and of phosphorylated ERK5 is decreased with bilateral EA "Zusanli" Point 30 min compared with trauma group.It is proved that traumatic stress may activate the expression of ERK1/2 and ERK5 as an external stimulus and increase the expression of its phosphorylation. EA bilateral "Zusanli" points can reduce the phosphorylation of ERK1/2 expression and phosphorylation of ERK5.Second, the impact on phosphorylated ERK1/2 and phosphorylated ERK5 by EA, and ERK5 inhibitor BIX02188After 24 h of trauma in rats, the expression of phosphorylated ERK5 is increased in the cerebral cortex than in normal control group (P<0.05,vs control) by western blot. The phosphorylation of ERK5 of EA group is lower than the expression of trauma model group (P<0.05). Intracerebroventricular injection of the inhibitor of ERK5 BIX02188 (4nmol or 20nmol) 30 min before trauma in rats, phosphorylation of ERK5 expression is significantly decreased than DMSO control group (P<0.01 vs DMSO), while the expression of phosphorylation of ERK1/2 in inhibitor group is not different with the DMSO group. It is also observed that after 24 h of trauma in rats, the expression of phosphorylated ERK1/2 is increased in the cerebral cortex, and electro-acupuncture group is decreased than in trauma group,which is the same as the way of immunohistochemistry. It is further confirmed that the expression of phosphorylated ERK1/2 and of phosphorylated ERK5 is increased after 24 h of trauma in rats, and EA can reduce its level of expression. BIX02188 can inhibit the phosphorylation of ERK5, whereas it has no effect on the phosphorylation ERK1/2.Third, the impact on natural killer (NK) cell activity by the EA or BIX02188 It is observed after 24 h of trauma in rats that the changes of the activity of natural killer (NK) cell and the impact by the EA or BIX02188. The activity of natural killer (NK) cell decreased, but the electro-acupuncture group increased than the trauma group. Intracerebroventricular injection of inhibitor of ERK5 BIX02188 (4nmol or 20nmol) 30min before trauma in rats, the inhibitor group (4nmol or 20nmol) increased than the trauma 1 group. The results showed that EA or ERK5 inhibitor BIX02188 (4nmol) can improve the activity of NK cell in the spleen after trauma.Fourth, the impact on proliferation of lymphocytes by the EA or BIX02188It is observed after 24 h of trauma in rats that the changes of proliferation of lymphocytes in the spleen and the impact by the EA or BIX02188. proliferation of lymphocytes decreased, but inhibitor of ERK5 BIX02188 (4nmol or 20nmol) group increased than the trauma group. The results showed that EA or ERK5 inhibitor BIX02188 (4nmol or 20nmol) can improve the proliferation of lymphocytes in the spleen after trauma.Summary:(1) After 24 h of trauma in rats, the expression of phosphorylated ERK1/2 and of phosphorylated ERK5 is increased in the cerebral cortex and EA bilateral "Zusanli" can reduce EA treatment the level of the expression.(2) The inhibitor of ERK5 BIX02188 (4nmol or 20nmol) can inhibit the phosphorylation of ERK5. BIX02188 can improve the immune suppression caused by traumatic stress.(3) EA may inhibit the phosphorylation of ERK5 cerebral cortex and ERK1/2 signaling pathway to improve the immune suppression caused by traumatic stress. |
