&lt;p&gt;Electroacupuncture Alleviates Spared Nerve Injury-Induced Neuropathic Pain And Modulates HMGB1/NF-κB Signaling Pathway In The Spinal Cord&lt;/p&gt;

Xia, Yang-yang; Xue, Meng; Wang, Ying; Huang, Zhihua; Huang, Cheng

doi:10.2147/jpr.s220201

Cited by 27 publications

(27 citation statements)

References 42 publications

(70 reference statements)

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“…In addition, HMGB1 could promote the production of proinflammatory cytokines by regulating TLR2 or TLR4, causing the activation of coagulation and microvascular thrombosis [48]. Moreover, HMGB1/NF-κB signaling has been widely reported in inflammation-associated acute injuries, including spared nerve injury [49], acute lung injury [50] and cerebral ischemia-reperfusion injury [51]. We demonstrated that miR-22-3p overexpression reduced the expression of p-65 and TLR4, accompanied by the inhibition of HMGB1, suggesting that miR-22-3p may reduce inflammatory response and apoptosis, in sepsis-induced kidney injury rat model and LPS induced cell injury model, through HMGB1/NF-κB pathway.…”

Section: Discussionmentioning

confidence: 99%

MiR-22-3p suppresses sepsis-induced acute kidney injury by targeting PTEN

Wang

Kong

et al. 2020

Bioscience Reports

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Background: Septic acute kidney injury is considered as a severe and frequent complication that occurs during sepsis. The present study was performed to understand the role of miR-22-3p and its underlying mechanism in sepsis-induced acute kidney injury. Methods: Rats were injected with adenovirus carrying miR-22-3p or miR-NC in the caudal vein before cecal ligation. Meanwhile, HK-2 cells were transfected with the above adenovirus following LPS stimulation. We measured the markers of renal injury (blood urea nitrogen (BUN), serum creatinine (SCR)). Histological changes in kidney tissues were examined by hematoxylin and eosin (H&E), Masson staining, periodic acid Schiff staining and TUNEL staining. The levels of IL-1β, IL-6, TNF-α and NO were determined by ELISA assay. Using TargetScan prediction and luciferase reporter assay, we predicted and validated the association between PTEN and miR-22-3p. Results: Our data showed that miR-22-3p was significantly down-regulated in a rat model of sepsis-induced acute kidney injury, in vivo and LPS-induced sepsis model in HK-2 cells, in vitro. Overexpression of miR-22-3p remarkably suppressed the inflammatory response and apoptosis via down-regulating HMGB1, p-p65, TLR4 and pro-inflammatory factors (IL-1β, IL-6, TNF-α and NO), both in vivo and in vitro. Moreover, PTEN was identified as a target of miR-22-3p. Furthermore, PTEN knockdown augmented, while overexpression reversed the suppressive role of miR-22-3p in LPS-induced inflammatory response. Conclusions: Our results showed that miR-22-3p induced protective role in sepsis-induced acute kidney injury may rely on the repression of PTEN.

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Section: Discussionmentioning

confidence: 99%

MiR-22-3p suppresses sepsis-induced acute kidney injury by targeting PTEN

Wang

Kong

et al. 2020

Bioscience Reports

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“…It is well known that EA stimulation served as an subsidiary therapy has been widely used to relieve neuropathic pain with fewer side effects [ 22 , 29 ]. Experiments demonstrated that EA stimulation has an inhibitory effect on mechanical hypersensitivity in spinal nerve ligation (SNL) rats [ 9 , 35 ].…”

Section: Discussionmentioning

confidence: 99%

“…Stimulation with 2 Hz EA alleviates SNL-induced neuropathic pain by promoting the occurrence of long-term depression (LTD) in the spinal dorsal horn [ 27 ]. Our previous studies have demonstrated that 2 Hz EA successfully ameliorated mechanical hypersensitivity through blockade of microglial activation and pro-inflammatory cytokine IL-1β production in the spinal cord of SNI rats [ 23 , 28 , 29 ], but the underlying mechanisms remain largely unknown. Based on the fact that neuroinflammatory response is regarded as a crucial role in the pathogenesis of neuropathic pain, including the alterations of pain-related signaling molecules [ 30 , 31 ], BDNF is known to be an endogenous neuromodulator in the nociceptive pathway and exerts a critical action via its interactions with TrκB receptor [ 8 ], and the BDNF/TrκB signaling pathway plays an important role in central sensitization and neuropathic pain development.…”

Section: Introductionmentioning

confidence: 99%

Electroacupuncture Modulates Spinal BDNF/TrκB Signaling Pathway and Ameliorates the Sensitization of Dorsal Horn WDR Neurons in Spared Nerve Injury Rats

Xue

Sun

Xia

et al. 2020

IJMS

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Neuropathic pain is more complex and severely affects the quality of patients’ life. However, the therapeutic strategy for neuropathic pain in the clinic is still limited. Previously we have reported that electroacupuncture (EA) has an attenuating effect on neuropathic pain induced by spared nerve injury (SNI), but its potential mechanisms remain to be further elucidated. In this study, we designed to determine whether BDNF/TrκB signaling cascade in the spinal cord is involved in the inhibitory effect of 2 Hz EA on neuropathic pain in SNI rats. The paw withdrawal threshold (PWT) of rats was used to detect SNI-induced mechanical hypersensitivity. The expression of BDNF/TrκB cascade in the spinal cord was evaluated by qRT-PCR and Western blot assay. The C-fiber-evoked discharges of wide dynamic range (WDR) neurons in spinal dorsal horn were applied to indicate the noxious response of WDR neurons. The results showed that 2 Hz EA significantly down-regulated the levels of BDNF and TrκB mRNA and protein expression in the spinal cord of SNI rats, along with ameliorating mechanical hypersensitivity. In addition, intrathecal injection of 100 ng BDNF, not only inhibited the analgesic effect of 2 Hz EA on pain hypersensitivity, but also reversed the decrease of BDNF and TrκB expression induced by 2 Hz EA. Moreover, 2 Hz EA obviously reduced the increase of C-fiber-evoked discharges of dorsal horn WDR neurons by SNI, but exogenous BDNF (100 ng) effectively reversed the inhibitory effect of 2 Hz EA on SNI rats, resulting in a remarkable improvement of excitability of dorsal horn WDR neurons in SNI rats. Taken together, these data suggested that 2 Hz EA alleviates mechanical hypersensitivity by blocking the spinal BDNF/TrκB signaling pathway-mediated central sensitization in SNI rats. Therefore, targeting BDNF/TrκB cascade in the spinal cord may be a potential mechanism of EA against neuropathic pain.

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“…Increasing evidence revealed that the inhibitory effect of EA stimulation is highly related to the modulation of neuroinflammation [17][18][19]. Our recent study demonstrated that 2 Hz EA alleviated SNIinduced neuropathic pain through blockade of microglial activation and proinflammatory cytokine IL-1β release in the spinal cord [20,21]. Other study also reported that CX3CR1 knockout mice exhibit the reduction of inflammatory and neuropathic pain and a decrease of spinal microglial response [22].…”

Section: Introductionmentioning

confidence: 77%

“…2 Hz EA treatment of SNI rats was conducted as previously described [20,21]. Briefly, rat was housed using a specially designed holder with its both hind legs and tail exposed; the skin of hind legs in the rat was sterilized using 75% alcohol.…”

Section: Electroacupuncture Stimulationmentioning

confidence: 99%

Electroacupuncture Treatment Suppresses Transcription Factor IRF8 in Spinal Cord of Rats with Spared Nerve Injury

Wang

Xue

Xia

et al. 2020

Pain Research and Management

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Objective. Neuropathic pain with complex mechanisms has become a major public health problem that greatly impacts patients’ quality of life. Therefore, novel and more effective strategies against neuropathic pain need further investigation. Electroacupuncture (EA) has an ameliorating effect on neuropathic pain following spared nerve injury (SNI), but the underlying mechanism remains to be fully clarified. Interferon regulatory factor 8 (IRF8), a critical transcription factor, was reported to be involved in the modulation of neuropathic pain. Here, we focused on exploring whether 2 Hz EA stimulation exerts an inhibitory action on spinal IRF8 in SNI rats. Methods. In this study, SNI rats were treated with 2 Hz EA once every other day for 21 days. Paw withdrawal threshold (PWT) was applied to determine the analgesic effect of 2 Hz EA on SNI rats. The spinal IRF8 and CX3CRl expressions were detected with qRT-PCR and western blot, and immunofluorescence staining was used to evaluate colocation of IRF8 or CX3CRl with microglial activation marker CD11b in the spinal cord. Results. It was found that SNI induced significant elevation of spinal IRF8 and CX3CRl mRNA and protein expression. Additionally, immunofluorescence results showed that SNI elicited the coexpression of IRF8 with CD11b, as well as CX3CRl with CD11b in the spinal cord. Meanwhile, 2 Hz EA treatment of SNI rats not only reduced IRF8 and CX3CRl mRNA and protein expression, but also reversed the coexpression of IRF8 or CX3CRl with CD11b in the spinal cord, along with an attenuation of SNI-evoked mechanical hypersensitivity. Conclusion. This experiment highlighted that 2 Hz EA can inhibit IRF8 expression and microglial activation in the spinal cord of SNI rats. Hence, targeting IRF8 may be a promising therapeutic strategy for 2 Hz EA treatment of neuropathic pain.

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<p>Electroacupuncture Alleviates Spared Nerve Injury-Induced Neuropathic Pain And Modulates HMGB1/NF-κB Signaling Pathway In The Spinal Cord</p>

Cited by 27 publications

References 42 publications

MiR-22-3p suppresses sepsis-induced acute kidney injury by targeting PTEN

MiR-22-3p suppresses sepsis-induced acute kidney injury by targeting PTEN

Electroacupuncture Modulates Spinal BDNF/TrκB Signaling Pathway and Ameliorates the Sensitization of Dorsal Horn WDR Neurons in Spared Nerve Injury Rats

Electroacupuncture Treatment Suppresses Transcription Factor IRF8 in Spinal Cord of Rats with Spared Nerve Injury

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