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Objectives: Osteoporosis is widely regarded as a typical aged-related disease caused by impaired bone remodeling. This research was designed to explore the protective effects of electroacupuncture (EA) on senile osteoporosis in a rat model and investigate the underlying mechanisms. Methods: Three-month-old rats were randomly selected as the youth group, and 24-month-old rats were randomly assigned to the elderly and EA groups. Rats in the EA group received 30 min of EA at bilateral SP10, ST36, K13 and GB34 daily, 5 days a week for 8 weeks. Bone mineral density (BMD), microstructure of the bone tissue, bone turnover biomarkers and expression level of autophagy-related proteins were detected. Results: Compared with the elderly group, EA treatment significantly increased BMD of the femur and ameliorated the microstructure. EA treatment increased trabecular bone volume ratio (= bone volume / total volume [BV/TV]) and trabecular number (Tb.N) and decreased trabecular separation (Tb.Sp) in senile osteoporosis rats. Compared with the elderly group, the serum N-terminal telopeptide of type I collagen (NTX1) level in the EA group was lower, and the serum procollagen type I N-terminal propeptide (PINP) concentration was higher. In addition, the expression of Beclin 1, microtubule-associated protein I light chain 3 (LC3B) and P62 was inhibited in the senile osteoporosis rats after EA treatment. Conclusions: EA can effectively alleviate aging-related bone loss and improve the microstructure of bone tissue in senile osteoporosis rats, and the regulation of autophagy might be one of the important mechanisms. [ABSTRACT FROM AUTHOR]

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)-1β, transforming growth factor (TGF)-β 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-1β 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. [ABSTRACT FROM AUTHOR]