Ozonated autohemotherapy combined with pulsed radiofrequency in the treatment of thoracic postherpetic neuralgia in older adults: a retrospective study.

Postherpetic neuralgia (PHN) seriously affects the quality of life of the elderly population. This study aimed to evaluate the efficacy of ozonated autohemotherapy (O3-AHT) combined with pulsed radiofrequency (PRF) in the treatment of thoracic PHN in older adults. The medical records of patients with thoracic PHN aged 65 years and older from June 2018 until March 2021 in Shengli Oilfield Central Hospital were reviewed. They were assigned into two groups: PRF alone (PRF group, n = 107) and PRF combined with O3-AHT (PRF + O3-AHT group, n = 109). Visual Analogue Scale for pain was evaluated at pre-treatment, 1 day, 1, 3 and 6 months after treatment. Quality of life and sleep quality were assessed using Short-Form 36 Health Survey and Athens Insomnia Scale at pre-treatment and 6 months post-treatment, respectively. The median age of patients in the PRF and PRF + O3-AHT groups were 69 (67-73) years and 68 (67-72) years, respectively. The former included 62 females and the latter included 51 females. Compared with pre-treatment, the Visual Analogue Scale scores of two groups declined at post-treatment. Patients in the PRF + O3-AHT group showed obviously lower Visual Analogue Scale scores compared with those in the PRF group at 1, 3, and 6 months after treatment and they had earlier withdrawal time for drugs. However, dizziness, tachycardia, sleepiness, and nausea were presented after combination therapy. These symptoms resolved spontaneously after a period of rest. Additionally, O3-AHT combined with PRF was associated with a significant decrease in the Athens Insomnia Scale score and with a significant improvement in every dimension of the Short-Form 36 Health Survey. To conclude, O3-AHT combined with PRF is an effective way to relieve thoracic PHN in older patients.

MiR-204-5p Alleviates Neuropathic Pain by Targeting BRD4 in a Rat Chronic Constrictive Injury Model.

Purpose: The pathogenesis of neuropathic pain is complex, and previous studies have found that microRNAs are important regulators of neuropathic pain and are associated with the progression of neuropathic pain. This study aims to explore the level and role of miR-204-5p in the chronic constrictive injury (CCI) model of rats. Patients and Methods: The CCI rat model was constructed to evaluate paw withdrawal threshold (PWT), paw withdrawal latency (PWL), the expressions of miR-204-5p, and the contents of inflammatory factors in the model. Overexpression of miR-204-5p in rat spinal cord was induced by intrathecal injection of miR-204-5p mimics. PWT and PWL were used to estimate mechanical and thermal pain thresholds. IL-6 and TNF-α were determined by ELISA. Luciferase reporter gene was conducted to verify the targeting relationship between miR-204-5p and BRD4. Results: miR-204-5p was abnormally down-regulated in the CCI group. The thresholds of mechanical and thermal pain stimulation in the CCI group were lower, and the levels of inflammatory factors were higher than those in the sham group. Overexpression of miR-204-5p alleviated PWT, PWL and inflammatory factors. Besides, the luciferase reporter gene showed that BRD4 was a target gene of miR-204-5p. Conclusion: These results suggested that miR-204-5p may alleviate neuropathic pain and inflammation through targeted regulation of BRD4 expression.

MicroRNA-448 modulates the progression of neuropathic pain by targeting sirtuin 1.

MicroRNAs (miRNAs) play crucial roles in the pathogenesis of neuropathic pain. The present study investigated the effects of miR-448 on the progression of neuropathic pain in a rat model of chronic constriction injury (CCI) of the sciatic nerve. Reverse-transcription quantitative polymerase chain reaction was conducted to detect the gene expression. The paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were used to assess the pain threshold. The protein expression levels of interleukin (IL)-6, IL-1ß and tumor necrosis factor-α (TNF-α) were detected by ELISA. The target of miR-448 was predicted by TargetScan software. The Student's t-test or one-way ANOVA were used to identify statistical differences among groups. miR-448 was persistently upregulated in CCI rats, and both mechanical allodynia and thermal hyperalgesia in CCI rats were decreased following miR-448 downregulation. The expression levels of IL-1ß, IL-6 and TNF-α were significantly increased in CCI rats compared with controls, and these effects were reversed following treatment with a miR-448 inhibitor. A luciferase reporter assay revealed that sirtuin 1 (SIRT1) was a target gene of miR-448. SIRT1 was found to abrogate the effect of miR-448 on neuropathic pain development. Collectively, the results of the present study revealed that miR-448 promoted neuropathic pain in CCI rats by regulating neuroinflammation via SIRT1. Therefore, SIRT1 may be considered as a novel biomarker for neuropathic pain.