BackgroundChronic obstructive pulmonary disease (COPD) is one of the most common lung diseases. It is a chronic inflammatory process characterised by airway obstruction and progressive lung inflammation, associated with difficulty breathing and insensitivity to corticosteroid therapy. Although there is some preliminary evidence to suggest a beneficial effect of acupuncture on COPD, its mechanism of action has not been investigated. Our aim was to examine the anti-inflammatory effects of acupuncture in a rat model of COPD induced by exposure to cigarette smoke (CS).MethodsSixty Sprague–Dawley rats were exposed to the smoke of 15 cigarettes for 1 h/day, 6 days/week for 3 months to induce COPD and treated with acupuncture at BL13 (Feishu), BL23 (Shenshu) and Dingchuan (COPD+Acupuncture, n=15), sham acupuncture (COPD+Sham, n=15) or left untreated (n=15). Exposed rats were compared with controls not exposed to CS (control, n=15). Pulmonary function was measured, and tumour necrosis factor-α (TNF-α) and interleukin-8 (IL-8) levels were determined in bronchoalveolar lavage fluid by ELISA. Histone deacetylase 2 (HDAC2) protein and mRNA expression were examined in lung tissue and in bronchus.ResultsAcupuncture treatment appeared to protect pulmonary function and reduce the COPD-induced inflammatory response by decreasing cell inflammation and the production of TNF-α and IL-8. Acupuncture also enhanced HDAC2 mRNA and protein expression, suggesting a possible direct effect on protein structure through post-translational modifications.ConclusionsOur results suggest that acupuncture regulates inflammatory cytokines and contributes to lung protection in a rat model of smoke-induced COPD by modulating HDAC2.

Acupuncture has been indispensable in Chinese medicine. However, its function still remains elusive. This paper studies the effect of acupuncture in ischemia stroke treatment using the Sprague Dawley rat animal model. We induced focal cerebral ischemia in rats using the middle cerebral artery occlusion (MCAO) procedure. For each rat in the real acupuncture group (n = 63), the sham acupoint treatment group (n = 62), and the blank control group (n = 30), we acquired 3-D fluorodeoxyglucose-microPET images at baseline, after MCAO, and after treatment, respectively. Then, we measured the changes of the injury-volume in the right hemisphere of these rats. The measurements showed that real acupuncture slightly reduced the injury-volume, sham acupoint treatment increased the injury-volume, and blank control had no obvious effect in reducing the injury-volume. Statistical tests also confirmed that acupuncture was more effective than random stimulus in improving the metabolic recovery after stroke.

Abstract. Long non-coding RNA (lncRNA) is a class of regulative non-coding RNA that is >200 nucleotides in length. Previous studies have demonstrated that lncRNA Fer-1-like family member 4 (FER1L4) serves regulatory roles in tumor progression; however, its clinical significance in human neuroglioma remains unclear. In the present study, data from The Cancer Genome Atlas was mined in order to investigate the association between FER1L4 expression and prognosis in patients with glioma. A short interfering (si)RNA targeting FER1L4 was transfected into U373-MG and U251 glioma cell lines, and cell viability, invasion and apoptosis were examined using CCK-8, Transwell and Annexin V-fluorescein isothiocyanate/propidium iodide assays, respectively. FER1L4 was significantly upregulated in high-grade glioma compared with low-grade glioma. Additionally, high expression of FER1L4 significantly predicted poor prognosis in patients with glioma. The expression of FER1L4 in glioma cell lines was significantly higher compared with that in normal astrocytes. Furthermore, by downregulating FER1L4 using siRNA, the invasiveness and viability of the glioma cells significantly decreased, while apoptosis significantly increased. The findings from the present study indicate that FER1L4 serves a role in the occurrence and progression of glioma, and could be used as a prognostic biomarker for this disease.

Moxibustion is the main alternative medicine treatment that has been beneficial to diabetic peripheral neuropathy (DPN), a common complication secondary to diabetic microvascular injury. However, the underlying protective mechanism of moxibustion against neuroinflammation remains unclear. We hypothesized that moxibustion treats DPN by regulating the balance of nuclear factor-2 erythroid-related factor-2 (Nrf2)-nuclear factor-kappa light chain enhancer of B cells (NF-кB). In vivo, diabetes was induced in rats by injecting streptozotocin (STZ; 60 mg/kg; i.p.). Moxibustion was then applied to “Zusanli” (ST 36), “Guanyuan” (BL 26), and “Yishu” (EX-B 3) acupuncture points. Nerve conduction was detected. Serum interleukin (IL)-1β, IL-6, and IL-8 levels were determined through enzyme-linked immunosorbent assay. NF-κB and Nrf2 proteins were examined through immunoblot analysis. The mRNA of NF-κB and Nrf2 was evaluated through RT-PCR. We found that the conduction velocity and amplitude of the action potentials of sciatic nerve conduction were reduced in the DPN model group but were rescued by moxibustion treatment. Moxibustion also improved the effect of DPN on other parameters, including ultrastructural changes, NF-κB and Nrf2 expression in the sciatic nerve, and serum IL-1β, IL-6, and IL-8 levels. Our data suggested that moxibustion may alleviate neuroinflammation by inhibiting NF-κB and by activating Nrf2. Moxibustion may also provide therapeutic effects for patients with DPN by simultaneously targeting Nrf2 and NF-κB.

Electroacupuncture (EA) therapy has been widely accepted as a useful therapeutic technique with low or no risk in the clinical prevention of cardiac hypertrophy. However, the signaling transduction mechanism underlying this effect remains unclear. The current study investigates the effects of EA on the signaling pathways of myocardial hypertrophy (MH) in rats. Up to 40 3-month-old Sprague-Dawley (SD) rats were randomly divided into normal, model, PC6 (Neiguan), and LI4 (Hegu) groups, with ten rats in each group. All the rats except for the normal group received 3 mg/kg·d of isoprinosine hydrochloride (ISO) injection into the back skin. The rats in the PC6 and LI4 groups received EA for 14 days. On the 15th day, electrocardiograms were recorded, and the ultrastructure of the myocardial cells was observed. The myocardial hypertrophy indices (MHIs), electrocardiograph (ECG), ultrastructure observation, levels of plasma angiotensin II (Ang II) and endothelin (ET), as well as protein expression of extracellular signal-regulated kinase (ERK), and phosphorylation extracellular signal regulating kinase (p-ERK) in the left ventricular myocardial tissue were measured. The results indicated that EA can improve cardiac function in MH rats by modulating upstream neuroendocrine cytokines that regulate the ERK signaling pathways.