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Poptotic cells. Interestingly, complement also plays a role in T and B cell activation and complement deficiency may disrupt the balance of lymphoid cell activation. Deficiencies of the classical complement component pathway are likely to affect SLE pathogenesis by decreasing clearance of apoptotic cell debris and immune complexes (IC), resulting in increased self-antigen availability, and dysregu
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Atment with a CRH antagonists, astressin and an ACTH antagonist, ACTH(11?4), prevented EA anti-edema. Taken together, these results suggest that in pathological conditions EA activates the HPA axis to increase CRH, ACTH, and glucocorticoid secretion and suppress inflammatory responses. It should be mentioned that EA significantly increased plasma ACTH levels in inflamed rats but not in naive rats,
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Than do healthy rats [23], it is possible that although EA does not produce stress in naive rats it may induce stress in inflamed rats. However, our previous study demonstrated that the same stimulation intensity at acupoint GB30 as that used in this study did not significantly change heart rate or blood pressure, both of which are indicators of stress response, in CFA-inflamed animals [2]. This s
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