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Browsing by Author "Du, Junying"
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Item Effects of low- and high-frequency electroacupuncture on protein expression and distribution of TRPV1 and P2X3 in rats with peripheral nerve injury(Sage, 2021-10) Du, Junying; Fang, Junfan; Xiang, Xuaner; Yu, Jie; Le, Xiaoqin; Liang, Yi; Jin, Xiaoming; Fang, Jiaoqiao; Anatomy and Cell Biology, School of MedicineBackground: Whether electroacupuncture (EA) stimulation at different frequencies has a similar effect on spared nerve injury (SNI) as other neuropathic pain models, and how EA at different frequencies causes distinct analgesic effects on neuropathic pain is still not clear. Methods: Adult male Sprague-Dawley rats were randomly divided into sham SNI, SNI, 2 Hz, 100 Hz and sham EA groups. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were measured. EA was performed once a day on days 1 to 14 after SNI. The expressions of transient receptor potential cation subfamily V member 1 (TRPV1) and peripheral purinergic P2X receptor 3 (P2X3) were determined by western blotting and immunofluorescence. TRPV1 siRNA and P2X3 siRNA were administered by intrathecal injection. TRPV1 or P2X3 agonists were combined with EA. Results: There were significant decreases in PWT, but no changes in PWL in the 14 days after SNI. EA using 2- or 100-Hz stimulation similarly increased PWT at every time point. The cytosol protein expression of P2X3 in the L4–L6 dorsal root ganglia (DRG) increased, but the expression of TRPV1 decreased in the SNI model. Both these effects were ameliorated by EA, with 2-Hz stimulation having a stronger effect than 100-Hz stimulation. Blocking either TRPV1 or P2X3 specific siRNAs attenuated the decreased PWT induced by SNI. Administration of either a TRPV1 or P2X3 agonist inhibited EA analgesia. Conclusion: 2- and 100-Hz EA similarly induced analgesic effects in SNI. This effect was related to up-regulation and down-regulation, respectively, of cytosol protein expression of P2X3 and TRPV1 in L4–L6 DRG, with 2 Hz having a better effect than 100 Hz.Item Electroacupuncture Alleviates Anxiety-like Behavior in Pain Aversion Rats by Attenuating the Expression of Neuropeptide Y in Anterior Cingulate Cortex(Elsevier, 2022) Shao, Fangbing; Du, Junying; Wang, Sisi; Cerne, Rok; Fang, Junfan; Shao, Xiaomei; Jin, Xiaoming; Fang, Jianqiao; Anatomy, Cell Biology and Physiology, School of MedicineBackground: Pain is considered as a multidimensional conscious experience that includes a sensory component and a negative affective-motivational component. Electroacupuncture (EA) is widely used to treat pain and pain-induced negative emotions, however, little is known about the mechanisms underlying the effect of EA. Objective: This study investigated the effect of EA on alleviating the anxiety-like behaviors in pain aversion rats and its anterior cingulate cortex (ACC) regulation mechanism. Methods: After a Freund's complete adjuvant (CFA)-conditioned place aversion (C-CPA) model was established in rats, EA treatment (2/100 Hz, 30 min, once/day, 4 days totally) was applied at bilateral Zusanli (ST36) and Kunlun (BL60) acupoints. Von Frey filaments were used to measure changes of pain withdrawal threshold (PWT) at indicated time points. Elevated zero maze (EZM) was used to investigate the changes of pain-related anxiety and CPA was used to investigate the changes of pain aversion. The protein expression levels of GAD67, PV, and NPY in ACC were detected by Western blotting. Results: Compared with the control group, the staying time in the "CFA-paired compartment" was significantly reduced, and the PWT was decreased in model group. In the EZM assessment, the distance and the time in open arm, as well as the number of open arm entries of model group were significantly lower than those in the control group. In the CPA assessment, the time spent in the "CFA-paired compartment" was significantly decreased in model group compared with control group, and EA reversed the changes in pain sensation and in pain-related emotions. Western blotting showed that the NPY level, but not the levels of GAD67 and PV, was significantly increased in the ACC of the model group compared to that of the control group. The increased expression of NPY in the ACC was significantly downregulated by EA, while sham EA produced no such effect. Conclusion: EA can effectively relieve the pain and pain-related emotions, and its mechanism may be achieved by down-regulating the expression of NPY in the ACC.Item Electroacupuncture Alleviates Anxiety-Like Behaviors Induced by Chronic Neuropathic Pain via Regulating Different Dopamine Receptors of the Basolateral Amygdala(Springer, 2022) Wu, Mengwei; Chen, Yeqing; Shen, Zui; Zhu, Yichen; Xiao, Siqi; Zhu, Xixiao; Wu, Zemin; Liu, Jinggen; Xu, Chi; Yao, Pingan; Xu, Weiwei; Liang, Yi; Liu, Boyi; Du, Junying; He, Xiaofen; Liu, Boyu; Jin, Xiaoming; Fang, Jianqiao; Shao, Xiaomei; Anatomy, Cell Biology and Physiology, School of MedicineChronic pain, such as neuropathic pain, causes anxiety and other negative emotions, which aggravates the pain sensation and increases the risk of chronic pain over time. Dopamine receptor D1 (DRD1) and dopamine receptor D2 (DRD2) in the basolateral amygdala (BLA) have been implicated in mediating anxiety-related behaviors, but their potential roles in the BLA in neuropathic pain-induced anxiety have not been examined. Electroacupuncture (EA) is commonly used to treat chronic pain and emotional disorders, but it is still unclear whether EA plays a role in analgesia and anxiety relief through DRD1 and DRD2 in the BLA. Here, we used western blotting to examine the expression of DRD1 and DRD2 and pharmacological regulation combined with behavioral testing to detect anxiety-like behaviors. We observed that injection of the DRD1 antagonist SCH23390 or the DRD2 agonist quinpirole into the BLA contributed to anxiety-like behaviors in naive mice. EA also activated DRD1 or inhibited DRD2 in the BLA to alleviate anxiety-like behaviors. To further demonstrate the role of DRD1 and DRD2 in the BLA in spared nerve injury (SNI) model-induced anxiety-like behaviors, we injected the DRD1 agonist SKF38393 or the DRD2 antagonist sulpiride into the BLA. We found that both activation of DRD1 and inhibition of DRD2 could alleviate SNI-induced anxiety-like behaviors, and EA had a similar effect of alleviating anxiety. Additionally, neither DRD1 nor DRD2 in the BLA affected SNI-induced mechanical allodynia, but EA did. Overall, our work provides new insights into the mechanisms of neuropathic pain-induced anxiety and a possible explanation for the effect of EA treatment on anxiety caused by chronic pain.Item Electroacupuncture Regulates Pain Transition Through Inhibiting PKCε and TRPV1 Expression in Dorsal Root Ganglion(Frontiers Media, 2021-07-20) Fang, Junfan; Wang, Sisi; Zhou, Jie; Shao, Xiaomei; Sun, Haiju; Liang, Yi; He, Xiaofen; Jiang, Yongliang; Liu, Boyi; Jin, Xiaoming; Fang, Jianqiao; Du, Junying; Anatomy and Cell Biology, School of MedicineMany cases of acute pain can be resolved with few side effects. However, some cases of acute pain may persist beyond the time required for tissue injury recovery and transit to chronic pain, which is hard to treat. The mechanisms underlying pain transition are not entirely understood, and treatment strategies are lacking. In this study, the hyperalgesic priming model was established on rats to study pain transition by injection of carrageenan (Car) and prostaglandin E2 (PGE2). The expression levels of protein kinase C epsilon (PKCε) and transient receptor potential vanilloid 1 (TRPV1) in the L4-L6 dorsal root ganglion (DRG) were investigated. Electroacupuncture (EA) is a form of acupuncture in which a small electric current is passed between a pair of acupuncture needles. EA was administrated, and its effect on hyperalgesia and PKCε and TRPV1 expression was investigated. The PKCε-TRPV1 signaling pathway in DRG was implicated in the pain transition. EA increased the pain threshold of model animals and regulated the high expression of PKCε and TRPV1. Moreover, EA also regulated hyperalgesia and high TRPV1 expression induced by selective PKCε activation. We also found that EA partly increased chronic pain threshold, even though it was only administered between the Car and PGE2 injections. These findings suggested that EA could prevent the transition from acute to chronic pain by inhibiting the PKCε and TRPV1 expression in the peripheral nervous system.Item Role of GABAAR in the Transition From Acute to Chronic Pain and the Analgesic Effect of Electroacupuncture on Hyperalgesic Priming Model Rats(Frontiers Media, 2021-06-17) Wang, Sisi; Du, Junying; Xi, Danning; Shao, Fangbing; Qiu, Mengting; Shao, Xiaomei; Liang, Yi; Liu, Boyi; Jin, Xiaomin; Fang, Jianqiao; Fang, Junfan; Anatomy and Cell Biology, School of MedicineChronic pain is a costly health problem that impairs health-related quality of life when not effectively treated. Regulating the transition from acute to chronic pain is a new therapeutic strategy for chronic pain that presents a major clinical challenge. The underlying mechanisms of pain transition are not entirely understood, and strategies for preventing this transition are lacking. Here, a hyperalgesic priming model was used to study the potential mechanism by which γ-aminobutyric acid receptor type A (GABAAR) in the dorsal root ganglion (DRG) contributes to pain transition. Furthermore, electroacupuncture (EA), a modern method of acupuncture, was administered to regulate pain transition, and the mechanism underlying EA's regulatory effect was investigated. Hyperalgesic priming was induced by intraplanar injection of carrageenan (Car)/prostaglandin E2 (PGE2). The decrease in mechanical withdrawal threshold (MWT) induced by PGE2 returned to baseline 4 h after injection in NS + PGE2 group, and still persisted 24 h after injection in Car + PGE2 group. Lower expression of GABAAR in the lumbar DRG was observed in the model rats. Furthermore, activating or blocking GABAAR could reversed the long-lasting hyperalgesia induced by Car/PGE2 injection or produced a persistent hyperalgesia. In addition, GABAAR may be involved in Protein Kinase C epsilon (PKCε) activation in the DRG, a mark molecular of pain transition. EA considerably increased the mechanical pain thresholds of hyperalgesic priming model mammals in both the acute and chronic phases. Furthermore, EA upregulated the expression of GABAAR and inhibited the activation of PKCε in the DRG. In addition, peripheral administration of picrotoxin blocked the analgesic effect of EA on the model rats and abolished the regulatory effect of EA on PKCε activation. These findings suggested that GABAAR plays a key role in both the transition from acute to chronic pain and the analgesic effect of EA on hyperalgesic priming.