Electroacupuncture pretreatment protects septic rats from acute lung injury by relieving inflammation and regulating macrophage polarization.

BACKGROUND: Macrophage polarization toward the M2 phenotype may attenuate inflammation and have a therapeutic effect in acute lung injury (ALI). OBJECTIVE: To investigate the role of electroacupuncture (EA) pretreatment on the inflammatory response and macrophage polarization in a septic rat model of lipopolysaccharide (LPS)-induced ALI. METHODS: Male Sprague Dawley rats (n = 24) were randomly divided into three groups (n = 8 each): control (Ctrl), ALI (LPS) and pre-EA (LPS + EA pretreatment). ALI and pre-EA rats were injected with LPS via the caudal vein. Pulmonary edema was assessed by left upper pulmonary lobe wet-to-dry (W/D) ratios. Lung injury scores were obtained from paraffin-embedded and hematoxylin and eosin-stained sections of the left lower pulmonary lobe. Inflammatory activation was quantified using serum tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, transforming growth factor (TGF)-ß and IL-10 levels measured by enzyme linked immunosorbent assay (ELISA). Macrophage phenotype was determined by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting. RESULTS: Mean lung W/D ratio was significantly lower and serum IL-1ß levels were decreased in pre-EA rats compared to ALI rats (P < 0.05). TNF-α mRNA expression was decreased and mannose receptor (MR) and Arg1 mRNA expression was increased in the lung tissues of pre-EA rats compared to ALI rats (P < 0.01). Arg1 protein expression was similarly increased in the lung tissues of pre-EA rats compared to ALI rats (P < 0.05). CONCLUSION: EA pretreatment may play a protective role by promoting macrophage polarization to the M2 phenotype in a septic rat model of LPS-induced ALI.

Effect of the Pulsed Electromagnetic Field Treatment in a Rat Model of Senile Osteoporosis In Vivo.

This study assessed the effects of pulsed electromagnetic fields (PEMF) in a rat model of senile osteoporosis and the underlying molecular events. 24-month-old male Sprague-Dawley (SD) rats were randomly divided into control and PEMF groups (n = 8 per group) using a random digit table, while 3-month-old male SD rats were set as the young-age control group. Rats in the PEMF group were treated by PEMF for 40 min/day for 5 days/week. Bone mineral density/microarchitecture, level of serum bone-specific alkaline phosphatase (BALP), tartrate-resistant acid phosphatase 5b (TRACP5b), and Wnt/ß-catenin signaling genes in rat bone marrow cells were then analyzed. The 12-week PEMF intervention showed a significant effect on inhibition of age-induced bone density loss and deterioration of trabecular bone structures in the PEMF group rats versus control rats, that is, the treatment enhanced bone mineral density of the proximal femoral metaphysis and the fifth lumbar (L5) vertebral body and improved the proximal tibia and L4 vertebral body parameters using bone histomorphometry analysis. Furthermore, the BALP level in the bones was significantly increased, but the TRACP5b level was reduced in the PEMF group of rats versus control rats. PEMF also dramatically upregulated expression of Wnt3a, LRP5, ß-catenin, and Runx2 but downregulated PPAR-γ expression in the aged rats. The results demonstrated that PEMF could prevent bone loss and architectural deterioration due to the improvement of bone marrow mesenchymal stromal cell differentiation and proliferation abilities and activating the Wnt signaling pathway. Future clinical studies are needed to validate these findings. © 2022 Bioelectromagnetics Society.

Effects of Ultrashort Wave Therapy on Inflammation and Macrophage Polarization after Acute Lung Injury in Rats.

Acute lung injury (ALI) features dysregulated pulmonary inflammation. Ultrashort waves (USWs) exert anti-inflammatory effects but no studies have evaluated their activity in ALI. Herein, we used an in vivo lipopolysaccharide (LPS)-induced ALI model to investigate whether the anti-inflammatory activity of USWs is mediated by altering the polarization of M1 to M2 macrophages. Twenty-four male Sprague-Dawley rats were randomly divided into control, untreated ALI, and ALI treated with USW groups (n = 8 in each group). ALI was induced by intratracheal LPS instillation. Rats in the USW group were treated for 15 min at 0, 4, and 8 h after a single LPS intratracheal instillation. Histopathologic examination, wet/dry lung weight ratio, enzyme-linked immunosorbent assay, quantitative real-time polymerase chain reaction, and western blot analyses were performed to evaluate the degree of lung injury and to determine macrophage phenotypes. Histopathologic examination disclosed attenuation of ALI, with reduced alveolar hemorrhage and neutrophilic infiltration in the USW group. Serum levels of tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) were significantly decreased after USW therapy. Moreover, the messenger RNA (mRNA) expressions of TNF-α and IL-1ß were significantly decreased in the USW group, whereas the mRNA expression of Arginase 1 (Arg1) and the protein expression of mannose receptor significantly increased in comparison with the untreated ALI group. We conclude that USW therapy may attenuate inflammation in LPS-induced ALI through the modulation of macrophage polarization. © 2021 Bioelectromagnetics Society.