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Our study aimed to investigate the effect of electroacupuncture pretreatment on the inflammatory response and expression levels of LC3-II/I and Beclin 1 using a model of lipopolysaccharide (LPS)-induced acute lung injury (ALI). Eighteen male Sprague-Dawley (SD) rats were randomly divided into three groups: normal control group (NC, n = 6), LSP modeling group (LM, n = 6), and electroacupuncture group (EA, n = 6). Rats in the EA group received electroacupuncture pretreatment at bilateral Zusanli (ST36) and Chize (LU5) points for five days (30 min each time daily, frequency; 3 Hz/15 Hz, intensity; 1 mA). Rats in the EA and LM groups were then injected with 5 mg/kg LPS (Beijing, Solarbio Company, concentration; 5 mg/mL) through the tail vein, while those in the NC group were injected with 5 mg/kg saline. The animals were sacrificed six hours after LPS or saline injection through cervical vertebrae by dislocation under deep anesthesia. Orbital blood was collected for the analysis of serum inflammatory factors including interleukin-1β (IL-1β) and transforming growth factor-β (TGF-β). The lower left lung was excised, stained with hematoxylin-eosin (HE), and subjected to histopathological analysis. The mRNA and protein expression of Beclin 1 and LC3 II/I in the lower right lung tissues were detected via RT-qPCR and Western blot analyses, respectively. The results showed that lung injury score was significantly higher in the LM group than that of the NC group (P < 0.01) and EA group (P < 0.01). The IL-1β contents were significantly decreased in the EA group (P < 0.01) than in the LM group. In contrast, the GF-β contents were increased in the EA group significantly when compared with the LM group (P < 0.01). RT-qPCR and Western blot detection showed that the relative gene expression of LC3‐II/I and Beclin 1 was significantly lower in the EA group than in the LM group (P < 0.01). However, the relative protein expression level of LC3‐II/I and Beclin 1 was slightly lower in the EA group than the in LM group (P > 0.05). These results show that electroacupuncture pretreatment reduces the inflammatory response in ALI and can protect lung tissue by inhibiting the gene and protein expression levels of LC3‐II/I and Beclin 1. [ABSTRACT FROM AUTHOR]

Objective. The aim of the study is to explore the relationship between lymphatic metastasis genes, prognosis, and immune cell infiltration in patients with colon cancer. Methods. Based on the Cancer Genome Atlas Program (TCGA) database, differentially expressed genes and prognostic genes related to colon adenocarcinoma (COAD) lymphatic metastasis were screened and intersected. We used lasso and univariate Cox regression analysis to screen core genes and establish a preliminary prediction model. GO and KEGG enrichment analysis was used for lymphatic metastasis-related genes, and single GSEA was used for the final screening results. Finally, we evaluated the relationship between identified genes and immune cell infiltration. Results. A total of 1727 genes were differentially expressed between COAD patients with TNM stages of N0 and N1. After further screening, six core genes (RNU4-2, ZNF556, RNVU1-15, NSA2P6, RN7SL767P, and RN7SL473P) were obtained, and a preliminary prediction model was established, in which ZNF556 was a risk factor, and the rest were protective factors. Single GSEA showed that pathways such as systemic lupus erythematosus might play an important role in the initial lymphatic metastasis of COAD. GO and KEGG enrichment analysis of 1727 genes supported this result. Immune infiltration analysis showed that six genes were significantly correlated with T cell and NK cell families. Conclusion. Six core genes may affect COAD initial lymphatic metastasis through the systemic lupus erythematosus pathway and immune cell infiltration. [ABSTRACT FROM AUTHOR]

Electroacupuncture (EA) has been clinically used in knee osteoarthritis broadly and proved to be effective than other therapies with fewer side effects; however, the mechanism of electroacupuncture to work on cartilage remains unclear. In this study, we aimed to evaluate the effect of EA treatment on cartilage and the relationship between EA and proteins such as HIF-a and SOX9. EA (dilatational wave, 3–15 HZ, 1 mA) has been applied to bilateral Zusanli (ST36), Xuehai (SP10), Taixi (KI3), and Yanglingquan (GB34) of rats. Results showed that the cartilage of the knee osteoarthritis group had obvious damage and fissure formation while the EA group showed that the cartilage destruction was generally milder. In addition, the protein expression levels of HIF-1α, and chondrogenic markers such as Sox9, and ACAN in the electroacupuncture group were higher than those in the ACLT group. Also, the extracellular matrix protein expression levels of MMP13 and ADAMTS5 were decreased in the EA group. These findings indicate that EA could alleviate the severity of knee osteoarthritis, and HIF-a and SOX9 may closely attribute to the treatment. [ABSTRACT FROM AUTHOR]

Lead exposure causes or aggravates hearing damage to human or animal, but the detailed effects of lead exposure on auditory system including injury sites of the cochlea in mammal remain controversy. To investigate the effect of chronic lead exposure on auditory system, 40 adult guinea pigs with normal hearing were randomly divided into five groups. They were fed 2 mmol/L lead acetate in drinking water for 0, 15, 30, 60, and 90 days (n = 8), respectively. Lead concentrations in blood, cochlea, and brainstem were measured. Auditory function was measured by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE). The morphology of cochlea and brainstem was observed, and expression of autophagy-related protein in brainstem was also assessed. The blood lead concentration reached a high level at the 15th day and kept stable, but the lead level in brainstem and cochlear tissue increased obviously at the 60th day and 90th day of lead exposure, respectively. There was no significant difference in the morphology of hair cells and stria vascularis (SV) among these five groups, but the number of spiral ganglion neuron (SGN) gradually decreased after 60 days. The differences of ABR thresholds and DPOAE amplitudes were not statistically significant among each group, but I wave latency, III latency, and I-III wave interval of ABR were delayed with the prolonging of time of lead exposure. The expressions of autophagy-related protein ATG5, ATG6, and LC3B in brainstem were increased after 30 days. These results suggest that the key target of lead toxicity was the auditory nerve conduction pathway including SGNs and brainstem, rather than cochlear hair cells and SV. Autophagy may play a very important role in lead toxicity to auditory nervous system. [ABSTRACT FROM AUTHOR]

Background. ANLN and miR-30a-5p may be involved in the progression of lung adenocarcinoma (LUAD). However, their underlying mechanism in LUAD has not been completely comprehended. Methods. Differential expression analysis, binding site prediction, and survival analysis were conducted by bioinformatics approaches. ANLN mRNA and miR-30a-5p expression were detected by qRT-PCR. ANLN protein expression was detected by western blot. Cell behaviors in LUAD were examined by functional experiments. Results. ANLN was activated in LUAD cells in terms of mRNA and protein. High ANLN level was positively correlated with poor prognosis. Enforced ANLN stimulated protumorigenesis LUAD cell behaviors. miR-30a-5p could target ANLN mRNA, as revealed and verified through assays. Remarkably low miR-30a-5p expression was observed in LUAD cells, and it could repress ANLN expression. The accelerated cell behaviors by overexpression of ANLN were counteracted by upregulating miR-30a-5p. Conclusion. Overall, miR-30a-5p remarkably restrained the malignant progression of LUAD cells by constraining ANLN expression. Thus, ANLN and miR-30a-5p could be novel therapeutic targets of LUAD. [ABSTRACT FROM AUTHOR]