Points - Recent Research
Autonomically Mediated Anti-Inflammatory Effects of Electrical Stimulation at Acupoints in a Rodent Model of Colonic Inflammation
  Electroacupuncture Decreases Netrin-1-Induced Myelinated Afferent Fiber Sprouting and Neuropathic Pain Through μ-Opioid Receptors
  Stemona Alkaloids Suppress the Positive Fedback Loop Between M2 Polarization and Fibroblast Differentiation by Inhibiting JAK2/STAT3 Pathway in Fibroblasts and CXCR4/PI3K/AKT1 Pathway in Macrophages

Autonomically Mediated Anti-Inflammatory Effects of Electrical Stimulation at Acupoints in a Rodent Model of Colonic Inflammation

Jin H, et al.

BACKGROUND: Acupuncture has been widely accepted for treatments of many diseases. This study was performed to determine effects and mechanisms of electroacupuncture (EA) by chronically implanted electrodes at acupoint ST36 on colonic inflammation induced by TNBS in rats.
METHODS: After intrarectal administration of TNBS, the rats were treated with sham-EA, EA1/EA2 (two sets of parameters) for 3 weeks. Disease activity index (DAI), macroscopic and microscopic lesions, plasma levels of TNF-α, IL-1β and IL-6 were observed as evaluation of inflammatory responses. The autonomic function was assessed by analysis of the heart rate variability.
RESULTS:(a) Vagal activity was significantly increased with both acute and chronic EA1/EA2; (b) DAI was significantly decreased with both chronic EA1 and EA2, and EA2 was more potent than EA1 (P < 0.05); (c) The macroscopic score was 6.4 0.6 with sham-EA and reduced to 4.9 0.1 with EA1 (P < 0.05) and 4.0 0.2 with EA2 (all P < 0.05). The histological score was 4.05 0.58 with sham-EA and remained unchanged (3.71 0.28) with EA1 (P > 0.05) but reduced to 3.0 0.3 with EA2 (P < 0.01); (d) The plasma levels of TNF-α, IL-1β and IL-6 were significantly decreased with EA2.
CONCLUSIONS: Electrical stimulation at ST36 improves colonic inflammation in TNBS-treated rats by inhibiting pro-inflammatory cytokines via the autonomic mechanism.

Neurogastroenterol Motil. 2019 May 22:e13615. doi: 10.1111/nmo.13615. [Epub ahead of print]

Source: PubMed

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Electroacupuncture Decreases Netrin-1-Induced Myelinated Afferent Fiber Sprouting and Neuropathic Pain Through μ-Opioid Receptors

Li HP, et al.

Purpose: We determined whether electroacupuncture (EA) reduces Netrin-1-induced myelinated primary afferent nerve fiber sprouting in the spinal cord and pain hypersensitivity associated with postherpetic neuralgia (PHN) through activation of μ-opioid receptors. Methods: PHN was induced by systemic injection of resiniferatoxin (RTX) in rats. Thirty-six days after RTX injection, a μ-opioid receptor antagonist, beta-funaltrexamine (β-FNA) or a κ-opioid receptor antagonist, nor Binaltorphimine (nor-BNI), was injected intrathecally 30 mins before EA, once every other day for 4 times. Mechanical allodynia was tested with von Frey filaments. The protein expression level of Netrin-1 and its receptors (DCC and UNC5H2) were quantified by using western blotting. The myelinated primary afferent nerve fiber sprouting was mapped with the transganglionic tracer cholera toxin B-subunit (CTB). Results: Treatment with 2 Hz EA at "Huantiao" (GB30) and "Yanglingquan" (GB34) decreased the mechanical allodynia at 22 days and the myelinated primary afferent nerve fiber preternatural sprouting into the lamina II of the spinal dorsal horn at 42 days after RTX injection. Also, treatment with 2 Hz EA reduced the protein levels of DCC and Netrin-1 and promoted the expression of UNC5H2 in the spinal dorsal horn 42 days after RTX injection. Furthermore, the μ-opioid receptor antagonist β-FNA, but not the κ-opioid receptor antagonist nor-BNI, reversed the effect of EA on neuropathic pain caused by RTX. In addition, morphine inhibited the Netrin-1 protein level induced by RTX in SH-SY5Y cells. Conclusions: Through activation of μ-opioid receptors, treatment with EA reduces the expression level of DCC and Netrin-1 and changes a growth-permissive environment in spinal dorsal horn into an inhibitory environment by increasing UNC5H2, thus decreasing RTX-caused primary afferent nerve sprouting in the spinal dorsal horn and neuropathic pain

J Pain Res. 2019 Apr 23;12:1259-1268. doi: 10.2147/JPR.S191900. eCollection 2019.

Source: PubMed

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Stemona Alkaloids Suppress the Positive Fedback Loop Between M2 Polarization and Fibroblast Differentiation by Inhibiting JAK2/STAT3 Pathway in Fibroblasts and CXCR4/PI3K/AKT1 Pathway in Macrophages

Ding Q, et al.

This study aimed to investigate the interaction between macrophages and fibroblasts in pulmonary fibrosis and the effects of total alkaloids of Stemona tuberosa (STA, 9 alkaloids with relative content of 91.2%) on them. The culture medium of LPS- or IL-4-induced macrophages was used as conditioned medium (CM) to co-culture with fibroblasts to study the effect of macrophages on the differentiation of fibroblasts. Similarly,the CM of TGF-β1-induced fibroblasts was co-culture with macrophages to study the effect of fibroblasts on the polarization of macrophages. The results showed that the TGF-β1 level in IL-4-induced (M2) rather than LPS-induced (M1) macrophages was significantly high (p < 0.001), and the SDF-1 level in TGF-β1-induced fibroblasts (MF) was significantly high (p < 0.001). The expressions of α-SMA and Col-1 in M2-CM-induced fibroblasts and Arg-1 and CXCR4 in MF-CM-induced macrophages were significantly increased (p < 0.01). STA effectively decreased the expressions of α-SMA (p < 0.05, 0.01 at 10, 100 μg/mL), Col-1 (p < 0.05, 0.05, 0.01 at 1, 10, 100 μg/mL), Arg-1 (p < 0.01 at 1, 10, 100 μg/mL) and CXCR4 (p < 0.01, 0.001 at 10, 100 μg/mL), which were consistent with the experimental results in vivo. These results suggested that there was a positive feedback loop between M2 polarization and fibroblast differentiation in pulmonary fibrosis. Further studies showed that the transcription of sdf-1 gene in MF was initiated by JAK2/STAT3 pathway and the M2 polarization was promoted by SDF- 1/CXCR4/PI3K/AKT1 pathway. STA blocked the feedback loop by suppressing JAK2/STAT3 pathway in fibroblasts and CXCR4-PI3K/AKT1 pathway in macrophages.

Int Immunopharmacol. 2019 Apr 24;72:385-394. doi: 10.1016/j.intimp.2019.04.030. [Epub ahead of print]

Source: PubMed

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