Effects of Baduanjin on patients with chronic nonspecific low back pain: A randomized controlled trial.

BACKGROUND: Chronic low back pain (CLBP) is 1 of the common clinical diseases, and many treatment methods can only improve the symptoms of pain in the short term. Traditional Chinese sports - Baduanjin has been proven to have a positive effect on chronic low back pain. However, the quality of the research is low, the sample size is small, and safety observations are lacking. We describe the protocol of a randomized controlled trial to study the efficacy and safety of Baduanjin chronic low back pain. METHODS: This randomized, controlled, evaluator-blind, two-arm, parallel clinical trial will include 90 outpatients with chronic low back pain recruited from the First Hospital of Nanping City, Fujian Province. The patients were randomly assigned to the intervention group (Baduanjin exercise training) and the control group (not receiving any special exercise training) at a ratio of 1:1. Patients in the intervention group will receive Baduanjin exercise training 3 times a week for 24 weeks. The 2 groups received a 4- week follow-up observation at 24 weeks. The main result from the intervention before intervention to 24 weeks later, and the follow-up of 4 changes the visual analog scale score at weeks, and by independent t are tested groups. It will also review the Pain-related disability index, The Quebec Back Pain Disability Scale, Health-related quality of life, Roland Morris (Roland Morris) Disability Questionnaire, Overall Perceived Effect (OPE) and safety Compare. Cost data for cost-benefit and cost-benefit analysis will be collected. DISCUSSION: This will be the first study to compare the effectiveness and safety of Baduanjin for patients with chronic low back pain. The results may help healthcare professionals make clinical decisions and may reduce the cost of treatment for this disease. TRIAL REGISTRATION: ChiCTR2000033908.

Electroacupuncture inhibits annulus fibrosis cell apoptosis in vivo via TNF-α-TNFR1-caspase-8 and integrin ß1/Akt signaling pathways.

OBJECTIVE: To examine whether electroacupuncture (EA) treatment inhibited cell apoptosis of intervertebral annulus fibrosis (AF) via tumor necrosis factor-α (TNF-α)-tumor necrosis factor receptor 1 (TNFR1)-caspase-8 and integrin ß1/Akt signaling pathways in a rat model of cervical intervertebral disc degeneration caused by unbalanced dynamic and static forces. METHODS: Thirty-two Sprague-Dawley rats were included in this study, of which 24 rats underwent surgery to induce cervical intervertebral disc degeneration, while eight rats received EA treatment at Dazhui (GV 14). Immunohistochemical staining was used to detect TNF-α, TNFR1, and caspase-8. Apoptosis of AF cells was examined with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining. The mRNA and protein expression levels of integrin ß1 and Akt were evaluated with real-time polymerase chain reaction and western blot analysis, respectively. RESULTS: Treatment with EA decreased TUNEL-positive AF cells and lowered TNF-α, TNFR1 and caspase-8 positive cells compared with control groups. EA treatment also increased integrin ß1 and Akt mRNA and protein levels compared with controls. CONCLUSION: Treatment with EA inhibits AF cell apoptosis through suppression of the TNF-α-TNFR1-caspase-8 signal pathway and increases the expression of integrin ß1 and Akt. EA may be a good alternative therapy for treating cervical spondylosis.

Nitidine chloride inhibits hepatocellular carcinoma cell growth in vivo through the suppression of the JAK1/STAT3 signaling pathway.

Signal transducer and activator of transcription 3 (STAT3) is persistently activated in cancer cells and contributes to malignant progression in various types of cancer. The Janus-activated kinase (JAK) family phosphorylates STAT3 in response to stimulation by cytokines or growth factors. The JAK1-STAT3 signaling pathway plays an important role in cell proliferation and apoptosis. Nitidine chloride (NC) is a benzophenanthridine alkaloid that has been reported as an antitumor agent due to its its inhibitory effects on topoisomerase I. Using a mouse xenograft model of hepatocellular carcinoma (HCC), this study aimed to evaluate the effects of NC on tumor growth in vivo and to elucidate the underlying mechanisms. The analysis of the effects of NC on apoptosis in HCC tumor xenografts in mice was carried out by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay; the expression of Bcl-2, Bax, cyclin-dependent kinase (CDK)4, cyclin D1, p21 and proliferating cell nuclear antigen (PCNA) was analyzed by immunohistochemistry; and the protein expression of JAK1 and STAT3 was examined by western blot analysis. Our results revealed that treatment with NC decreased the tumor volume and tumor weight, suggesting that NC inhibits HCC cell growth in vivo. In addition, NC blocked the activation of JAK1-STAT3 in the tumor tissues, which in turn resulted in the induction of cancer cell apoptosis and the inhibition of proliferation. Consequently, treatment with NC downregulated the expression of cyclin D1, CDK4 and Bcl-2 and increased the level of p21 and Bax. Our data provide a molecular basis for the antitumor activity of NC.