Jinmaitong ameliorates diabetes-induced peripheral neuropathy in rats through Wnt/β-catenin signaling pathway

Song, Wei; Sun, Ying; Liang, Xuan; Zhang, Qian; Xie, Jun; Wang, Chao; Liu, Wei

doi:10.1016/j.jep.2020.113461

Cited by 8 publications

(5 citation statements)

References 44 publications

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“…The mechanism of QWZK protection against ALI induced by LPS may via inhibiting TLR4/NF-kB pathway and NLRP3 inflammasome activation and then downregulated the expression of IL-6, TNF-α, MCP-1, IL-1β, IL-18, and IFN-γ ( Figure 7 ). In present study, the effects of QWZK did not show good dose-effect manners, and similar phenomena were reported in previous studies ( Du et al, 2021 ; Pan et al, 2021 ; Song et al, 2021; Xie et al, 2022 ). The possible reason was the components of QWZK are complicated and diversiform, which acted by the mode of multi-component, multi-target and multi-action.…”

Section: Discussionsupporting

confidence: 92%

Qingwenzhike Prescription Alleviates Acute Lung Injury Induced by LPS via Inhibiting TLR4/NF-kB Pathway and NLRP3 Inflammasome Activation

Zhang

Wang

et al. 2021

Front. Pharmacol.

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Background: Acute lung injury (ALI) is characterized by dysfunction of the alveolar epithelial membrane caused by acute inflammation and tissue injury. Qingwenzhike (QWZK) prescription has been demonstrated to be effective against respiratory viral infections in clinical practices, including coronavirus disease 2019 (COVID-19) infection. So far, the chemical compositions, protective effects on ALI, and possible anti-inflammatory mechanisms remain unknown.Methods: In this study, the compositions of QWZK were determined via the linear ion trap/electrostatic field orbital trap tandem high-resolution mass spectrometry (UHPLC-LTQ-Orbitrap MS). To test the protective effects of QWZK on ALI, an ALI model induced by lipopolysaccharide (LPS) in rats was used. The effects of QWZK on the LPS-induced ALI were evaluated by pathological changes and the number and classification of white blood cell (WBC) in bronchoalveolar lavage fluid (BALF). To investigate the possible underlying mechanisms, the contents of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein (MCP-1), interleukin-1β (IL-1β), interleukin-18 (IL-18), and immunoregulatory-related factors interferon-γ (IFN-γ) were detected by ELISA. Furthermore, the expression of Toll-like receptor 4 (TLR4), p-IKKα/β, IKKα, IKKβ, p-IκBα, IκBα, p-NF-κB, nuclear factor-κB (NF-κB), NOD-like receptor family pyrin domain containing 3 (NLRP3), cleaved caspase-1, pro-caspase-1, apoptosis-associated speck-like protein containing CARD (ASC), and β-actin were tested by Western blot.Results: A total of 99 compounds were identified in QWZK, including 33 flavonoids, 23 phenolic acids, 3 alkaloids, 3 coumarins, 20 triterpenoids, 5 anthraquinones, and 12 others. ALI rats induced by LPS exhibited significant increase in neutrophile, significant decrease in lymphocyte, and evidently thicker alveolar wall than control animals. QWZK reversed the changes in WBC count and alveolar wall to normal level on the model of ALI induced by LPS. ELISA results revealed that QWZK significantly reduced the overexpression of proinflammatory factors IL-6, TNF-α, MCP-1, IL-1β, IL-18, and IFN-γ induced by LPS. Western blot results demonstrated that QWZK significantly downregulated the overexpression of TLR4, p-IKKα/β, p-IκBα, p-NF-κB, NLRP3, cleaved caspase-1, and ASC induced by LPS, which suggested that QWZK inhibited TLR4/NF-κB signaling pathway and NLRP3 inflammasomes.Conclusions: The chemical compositions of QWZK were first identified. It was demonstrated that QWZK showed protective effects on ALI induced by LPS. The possible underlying mechanisms of QWZK on ALI induced by LPS was via inhibiting TLR4/NF-kB signaling pathway and NLRP3 inflammasome activation. This work suggested that QWZK is a potential therapeutic candidate for the treatments of ALI and pulmonary inflammation.

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Section: Discussionsupporting

confidence: 92%

Qingwenzhike Prescription Alleviates Acute Lung Injury Induced by LPS via Inhibiting TLR4/NF-kB Pathway and NLRP3 Inflammasome Activation

Zhang

Wang

et al. 2021

Front. Pharmacol.

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“…This is achieved by increasing the content of insulin-like growth factor 1 (IGF-1), insulin-like growth factor 1 receptor (IGF-1R), myelin protein zero (MPZ), and peripheral myelin protein 22 (PMP22) expression, as well as related mRNAs in tissues under high glucose conditions (Song et al. 2019 , 2021 ).…”

Section: Methodsmentioning

confidence: 99%

Advances of traditional Chinese medicine preclinical mechanisms and clinical studies on diabetic peripheral neuropathy

Zhang,

Wu,

Yao

et al. 2024

Pharmaceutical Biology

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“…The rats were randomly divided into four groups ( n = 8) as follows: 1) Con (normal control rats that only received distilled water); 2) DM (diabetic rats that also received distilled water); 3) DM + JMT (diabetic rats that received 0.88 g/kg/d JMT, 10-fold the dosage for a human adult); 4) DM + ALA (diabetic rats that received 0.48 mmol/kg/d ALA). We chose the JMT dosage which showed the best neuroprotective effects in STZ-induced diabetic rats based on our previous studies ( Song et al, 2019 ; Song et al, 2021 ). ALA dosage chosen was based on published reports outlining STZ-induced diabetic rat models ( Lee et al, 2018 ; Sadeghiyan et al, 2019 ).…”

Section: Methodsmentioning

confidence: 99%

Jinmaitong Alleviates Diabetic Neuropathic Pain Through Modulation of NLRP3 Inflammasome and Gasdermin D in Dorsal Root Ganglia of Diabetic Rats

et al. 2021

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Jinmaitong (JMT) is a compound prescription of traditional Chinese medicine that has been used to treat diabetic neuropathic pain (DNP) for many years. Here, we investigated the effects of JMT on the activation of NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome and pyroptosis in Dorsal root ganglia (DRG) of diabetic rats. Streptozotocin (STZ)-induced diabetic rats were gavaged with JMT (0.88 g/kg/d) or alpha-lipoic acid (ALA, positive control, 0.48 mmol/kg/d) for 12 weeks. Distilled water was administered as a vehicle control to both diabetic and non-affected control rats. Blood glucose levels and body weights were measured. Behavioral changes were tested with mechanical withdrawal threshold (MWT) and tail-flick latency (TFL) tests. Morphological injury associated with DRG was observed with hematoxylin and eosin (H&E) and Nissl’s staining. mRNA and protein levels of NLRP3 inflammasome components (NLRP3, ASC, caspase-1), downstream IL-1β and gasdermin D (GSDMD) were evaluated by immunohistochemistry, quantitative real time-PCR and western blot. The results showed that JMT had no effect on blood glucose levels and body weights, but significantly improved MWT and TFL behavior in diabetic rats, and attenuated morphological damage in the DRG tissues. Importantly, JMT decreased the mRNA and protein levels of components of NLRP3 inflammasome, including NLRP3, ASC and caspase-1. JMT also down-regulated the expression of IL-1β and GSDMD in the DRG of DNP rats. In addition, ALA treatment did not perform better than JMT. In conclusion, JMT effectively relieved DNP by decreasing NLRP3 inflammasome activation and pyroptosis, providing new evidence supporting JMT as an alternative treatment for DNP.

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Jinmaitong ameliorates diabetes-induced peripheral neuropathy in rats through Wnt/β-catenin signaling pathway

Cited by 8 publications

References 44 publications

Qingwenzhike Prescription Alleviates Acute Lung Injury Induced by LPS via Inhibiting TLR4/NF-kB Pathway and NLRP3 Inflammasome Activation

Qingwenzhike Prescription Alleviates Acute Lung Injury Induced by LPS via Inhibiting TLR4/NF-kB Pathway and NLRP3 Inflammasome Activation

Advances of traditional Chinese medicine preclinical mechanisms and clinical studies on diabetic peripheral neuropathy

Jinmaitong Alleviates Diabetic Neuropathic Pain Through Modulation of NLRP3 Inflammasome and Gasdermin D in Dorsal Root Ganglia of Diabetic Rats

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