1.A clinical study on the treatment of refractory tennis elbow with arc-edge needle therapy based on zaodian theory
Xuejian MA ; Dongzhe ZHANG ; Chaoyang NIU ; Shuaigang DU ; Wuyang WANG ; Shilong CHENG ; Yingyuan XIAO ; Xuechang WANG
The Journal of Practical Medicine 2024;40(15):2161-2165
Objective To explore the clinical efficacy of arc-edge needle therapy based on Zaodian theory in the treatment of refractory tennis elbow.Methods 64 patients with refractory tennis elbow were collected and randomly divided into a control group and an observation group using a random number table method.Among them,32 cases in the control group were treated with local pain point injection.32 patients in the observation group were treated with arc-edge needle therapy once a week,with two treatments per group.The Number rating scale(NRS)Mayo,elbow joint performance score(MEPS)and Disabilities of the arm,shoulder and hand(DASH)score were recorded and compared between the two groups before treatment and at 1,2,4 and 24 weeks of follow-up after treatment,disease efficacy score(WDES)at 24 weeks of follow-up.Results During the treat-ment process,neither group of patients experienced serious adverse reactions.At each stage after treatment,two groups of NRS MEPS,DASH,and WDES at 24 weeks of follow-up all improved compared to before treatment.After one week of treatment,there was no statistically significant difference in NRS scores between the two groups(P>0.05).At follow-up visits at weeks 2,4,and 24,the NRS scores in the observation group were lower than those in the control group.After 1,2,4,and 24 weeks of follow-up after treatment,the DASH score was lower in the observation group than in the control group,and the MEPS score was higher in the observation group than in the control group,with statistically significant differences(P<0.05).After 24 weeks of treatment,the WDES of the observation group was better than that of the control group,and the difference was statistically significant(P<0.05).Conclusion Local pain point injection and arc-edge Zaodian release can alleviate pain and improve elbow joint function in the early stage of refractory tennis elbow.However,the long-term effect of local pain point injection treatment is not good,and the treatment effect of the observation group gradually improves.
2.Genistein attenuates LPS-induced inflammatory injury of rat dorsal root ganglion neuron via down-regulating HDAC6.
Songlin ZHOU ; Junqing HUANG ; Ke LI ; Shuaigang DU ; Bin YANG ; Zhonghua GUO
Journal of Central South University(Medical Sciences) 2022;47(6):707-716
OBJECTIVES:
Neuropathic pain (NP) is a chronic pain caused by somatosensory neuropathy or disease, and genistein (Gen) might be a potential drug for the treatment of NP. Therefore, this study aims to investigate the effect of Gen on lipopolysaccharide (LPS)-induced inflammatory injury of dorsal root ganglion neuron (DRGn) in rats and the possible molecular mechanism.
METHODS:
The DRGn of 1-day-old juvenile rats were taken for isolation and culture. The DRGn in logarithmic growth phase were divided into a control group, a LPS group, a tubastatin hydrochloride (TSA)+LPS group, a Gen1+LPS group, a Gen2+LPS group, a Gen2+LPS+TSA group, a Gen2+pcDNA-histone deacetylase 6 (HDAC6)+LPS group, and a Gen2+pcDNA3.1+LPS group. The LPS group was treated with 1 μg/mL LPS for 24 h; the TSA+LPS group, the Gen1+LPS group, the Gen2+LPS group were treated with 5 μmol/L TSA, 5 μmol/L Gen, 10 μmol/L Gen respectively for 0.5 h, and then added 1 μg/mL LPS for 24 h; the Gen2+TSA+LPS group was treated with 10 μmol/L Gen and 5 μmol/L TSA for 0.5 h and then added 1 μg/mL LPS for 24 h; the Gen2+pcDNA-HDAC6+LPS group and the Gen2+pcDNA3.1+LPS group received 100 nmol/L pcDNA-HDAC6 and pcDNA3.1 plasmids respectively, and 24 h after transfection, 10 μmol/L Gen was pretreated for 0.5 h, and then added 1 μg/mL LPS for 24 h. Real-time RT-PCR was used to detect the HDAC6 mRNA expression in DRGn; CCK-8 method was used to detect cell viability of DRGn; flow cytometry was used to detect cell apoptosis of DRGn; ELISA was used to detect the levels of IL-1β, IL-6, and TNF-α in DRGn culture supernatant; Western blotting was used to detect the protein expression of HDAC6, Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), and NF-κB p65 in DRGn.
RESULTS:
Compared with the control group, the expression levels of HDAC6 mRNA and protein, the expression levels of TLR4 and MyD88 protein in DRGn of LPS group rats were significantly up-regulated, the ratio of p-NF-κB p65/NF-κB p65 was significantly increased, and the activity of DRGn was significantly decreased, the apoptosis rate was significantly increased, and the levels of IL-1β, IL-6 and TNF-α in the DRGn culture supernatant were significantly increased (all P<0.05). Compared with the LPS group, the expression levels of HDAC6 mRNA and protein, TLR4 and MyD88 protein expression levels in DRGn of the TSA+LPS group, the Gen1+LPS group, the Gen2+LPS group and the Gen2+TSA+LPS group were significantly down-regulated, the ratio of p-NF-κB p65/NF-κB p65 was significantly decreased, the activity of DRGn was significantly increased, the apoptosis rate was significantly decreased, and the levels of IL-1β, IL-6 and TNF-α in the DRGn culture supernatant were significantly decreased (all P<0.05), and the above changes were most obvious in the Gen2+TSA+LPS group. Compared with the Gen2+LPS group, the expression levels of HDAC6 mRNA and protein, TLR4 and MyD88 protein expression levels in DRGn of the Gen2+pcDNA-HDAC6+LPS group were significantly up-regulated, the ratio of p-NF-κB p65/NF-κB p65 was significantly increased, the activity of DRGn was significantly decreased, and the apoptosis rate was significantly increased, and the levels of IL-1β, IL-6 and TNF-α in the DRGn culture supernatant were significantly increased (all P<0.05).
CONCLUSIONS
Gen can alleviate LPS-induced DRGn inflammatory injury in rats, which might be related to down-regulating the expression of HDAC6 and further inhibiting the activation of TLR4/MyD88/NF-κB signaling pathway.
Animals
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Ganglia, Spinal
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Genistein/pharmacology*
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Histone Deacetylase 6/metabolism*
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Interleukin-6/metabolism*
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Lipopolysaccharides
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Myeloid Differentiation Factor 88
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NF-kappa B/metabolism*
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Neurons/metabolism*
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RNA, Messenger
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Rats
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Toll-Like Receptor 4/metabolism*
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Tumor Necrosis Factor-alpha/metabolism*