Electroacupuncture inhibits apoptosis of splenic lymphocytes in traumatized rats through modulation of the TNF-α/NF-κB signaling pathway

Abstract

Surgical trauma leads to a severe deterioration of the immune system. Electroacupuncture (EA) may improve the immunodeficiency that occurs following surgery; however, the underlying signaling mechanisms require further study. In the present study, 40 rats were equally randomized into four groups: Control; Control + EA; Trauma; Trauma + EA. EA was applied at the 'Zusanli' (ST36) and 'Lanwei' (Extra37) acupoints, immediately following surgery. The splenic T cells were isolated from the rats 24 h after surgery. The apoptotic rate of the lymphocytes was measured by flow cytometric analysis, and western blotting was used to determine the protein expression levels of caspase-3, caspase-8, tumor necrosis factor (TNF)-α and TNF receptor 1 (TNFR1). The DNA binding activity of nuclear factor (NF)-κB was determined using Trans-AM® ELISA-based kits. The results of the present study showed that surgical trauma induced apoptosis of splenic lymphocytes, and significantly increased the protein expression levels of caspase-3 and caspase-8. This was accompanied by increased expression levels of TNF-α and TNFR1, and a marked reduction in the activity of NF-κB in splenic T cells. Administration of EA significantly decreased the expression levels of caspase-3, caspase-8, TNF-α and TNFR1, elevated the activity of NF-κB, and suppressed the apoptotic rate of the lymphocytes. The data suggests that EA may inhibit the apoptosis of splenic lymphocytes induced by surgical trauma, and ameliorate the postoperative immunosuppression. This may be mediated by the downregulation of TNF-α expression levels and upregulation of the activity of NF-κB.

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Effect of perioperative acupoint electrical stimulation on macrophages in mice under operative stress

“…NF-κB is a key transcription factor of stress and injury in eukaryotic cells, which is involved in normal activities and disease processes of the body, involving growth and development, cell differentiation, apoptosis, immune response, inflammatory response, trauma, stress Inflammation, tumor growth, chronic inflammatory diseases and other processes [ 16 , 17 ]. NF-κB can be activated by a variety of stimuli, it is the central regulator of innate immunity and acquired immunity, it can regulate the expression of various pro-inflammatory factors and anti-apoptotic proteins[ 16 ], and its nuclear translocation appears in normal animals Daily rhythm, the transcriptional activity of NF-κB is inhibited by increasing endogenous corticosterone under mild stress [ 17 ].…”

“…NF-κB is a key transcription factor of stress and injury in eukaryotic cells, which is involved in normal activities and disease processes of the body, involving growth and development, cell differentiation, apoptosis, immune response, inflammatory response, trauma, stress Inflammation, tumor growth, chronic inflammatory diseases and other processes [ 16 , 17 ]. NF-κB can be activated by a variety of stimuli, it is the central regulator of innate immunity and acquired immunity, it can regulate the expression of various pro-inflammatory factors and anti-apoptotic proteins[ 16 ], and its nuclear translocation appears in normal animals Daily rhythm, the transcriptional activity of NF-κB is inhibited by increasing endogenous corticosterone under mild stress [ 17 ]. Current research shows that glucocorticoid induces NF-κB gene transcription in two ways, one is through protein–protein interaction, in the nucleus, glucocorticoid-glucocorticoid receptor complex and NF- κB active p65 subunit of κB interacts and prevents the binding of transcriptionally active NF-κB and DNA recognition structures in the promoter region of the gene of interest.…”