Combined Rosiglitazone and Forskolin Have Neuroprotective Effects in SD Rats after Spinal Cord Injury

Meng, Qingqi; Lei, Wei; Chen, Hao; Feng, Zhencheng; Hu, Liqiong; Zhang, Xingliang; Li, Siming

doi:10.1155/2018/3897478

Cited by 9 publications

(8 citation statements)

References 38 publications

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“…We have previously reported that the PPAR- γ ligand, rosiglitazone, promotes functional recovery after SCI by blocking the loss of local neurons and decreasing NF- κ B expression [18, 19]. Loss of local neurons from SCI is largely induced by persistent inflammation.…”

Section: Introductionmentioning

confidence: 99%

PPAR-γ Activation Exerts an Anti-inflammatory Effect by Suppressing the NLRP3 Inflammasome in Spinal Cord-Derived Neurons

Meng

Feng

Zhang

et al. 2019

Mediators of Inflammation

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Persistent inflammation disrupts functional recovery after spinal cord injury (SCI). Peroxisome proliferator-activated receptor gamma (PPAR-γ) activation promotes functional recovery in SCI rats by inhibiting inflammatory cascades and increasing neuronal survival. We sought to clarify the relationship between PPAR-γ activation and NACHT, LRR and PYD domain-containing protein 3 (NLRP3) inflammasome suppression, and the role of NF-κB in activating the NLRP3 inflammasome in neurons. In SCI rats, we found that rosiglitazone (PPAR-γ agonist) inhibited the expression of caspase-1. In in vitro neurons, G3335 (PPAR-γ antagonist) reversed the rosiglitazone-induced inhibition of caspase-1, interleukin 1 (IL-1β), and interleukin 6 (IL-6). Rosiglitazone inhibited the expression of NLRP3, caspase-1, IL-1β, and IL-6. However, the activator of NLRP3 could counteract this inhibition induced by PPAR-γ activation. NF-κB did not participate in the process of rosiglitazone-induced inhibition of NLRP3. Consistent with our in vitro results, we verified that locomotor recovery of SCI rats in vivo was regulated via PPAR-γ, NLRP3, and NF-κB. These results suggest that PPAR-γ activation exerts an anti-inflammatory effect by suppressing the NLRP3 inflammasome—but not NF-κB—in neurons and that PPAR-γ activation is a promising therapeutic target for SCI.

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Section: Introductionmentioning

confidence: 99%

PPAR-γ Activation Exerts an Anti-inflammatory Effect by Suppressing the NLRP3 Inflammasome in Spinal Cord-Derived Neurons

Meng

Feng

Zhang

et al. 2019

Mediators of Inflammation

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“…The drug binds to the peroxisome proliferator-activated receptors in adipocytes and renders the cells more responsive to insulin. The neuroprotective effect of Rosiglitazone and other thiazolidinediones has been studied extensively and a beneficial effect has been suggested through inhibition of inflammatory responses, pro-apoptotic cascades, and mitochondrial metamorphosis [32][33][34].…”

Section: Discussionmentioning

confidence: 99%

Comparison of Glaucoma-Relevant Transcriptomic Datasets Identifies Novel Drug Targets for Retinal Ganglion Cell Neuroprotection

Enz

Tribble

Williams

2021

JCM

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Glaucoma is a leading cause of blindness and is characterized by the progressive dysfunction and irreversible death of retinal ganglion cells. We aimed to identify shared differentially expressed genes (DE genes) between different glaucoma relevant models of retinal ganglion cell injury using existing RNA-sequencing data, thereby discovering targets for neuroprotective therapies. A comparison of DE genes from publicly available transcriptomic datasets identified 12 shared DE genes. The Comparative Toxicogenomics Database (CTD) was screened for compounds targeting a significant proportion of the identified DE genes. Forty compounds were identified in the CTD that interact with >50% of these shared DE genes. We next validated this approach by testing select compounds for an effect on retinal ganglion cell survival using a mouse retinal explant model. Folic acid, genistein, SB-431542, valproic acid, and WY-14643 (pirinixic acid) were tested. Folic acid, valproic acid, and WY-14643 demonstrated significant protection against retinal ganglion cell death in this model. The increasing prevalence of open access-omics data presents a resource to discover targets for future therapeutic investigation.

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“…Rosiglitazone is a clinical drug for type 2 diabetes that exhibits the potential to inhibit the inflammatory response [ 19 ]. It has been reported that rosiglitazone has a positive effect in reducing intestinal inflammation in various experimental models [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

Rosiglitazone ameliorates radiation-induced intestinal inflammation in rats by inhibiting NLRP3 inflammasome and TNF-α production

Chen

Zhang

et al. 2020

Journal of Radiation Research

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Radiation-induced acute intestinal injury is a common and serious occurrence following abdominal and pelvic irradiation. The Nod-like receptor protein 3 (NLRP3)-dependant inflammasome and inflammation activation is crucial in this process. In a pre-experimental design of radiation-induced intestinal injury, we found that rosiglitazone inhibited caspase-1 which is a key marker of inflammasome activation. The purpose of the present study was to clarify the inhibitory effect of rosiglitazone on the NLRP3 inflammasome both in vivo and in vitro. Radiation-induced intestinal injury after rosiglitazone treatment, and the expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), caspase-1 and NLRP3 in a radiation-induced intestinal injury model in a rat and macrophages were observed. We found that rosiglitazone ameliorated radiation-induced intestinal injury in rats by suppressing the expression of caspase-1, NLRP3, IL-1β and TNF-α. Treatment with rosiglitazone in vitro reduced the expression of NLRP3, and the NLRP3 activator monosodium urate (MSU) reversed the inhibition of IL-1β and TNF-α by rosiglitazone in macrophages. MSU reversed the protective effect of rosiglitazone on radiation-induced intestinal injury in rats by reversing the rosiglitazone-induced inhibition of IL-1β and TNF-α. Taken together, these findings indicate that the peroxisome proliferator-activated receptor gamma (PPARγ) agonist, rosiglitazone, ameliorates radiation-induced intestine inflammation in rats via inhibiting the induction of the NLRP3-dependent inflammasome in macrophages.

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Combined Rosiglitazone and Forskolin Have Neuroprotective Effects in SD Rats after Spinal Cord Injury

Cited by 9 publications

References 38 publications

PPAR-γ Activation Exerts an Anti-inflammatory Effect by Suppressing the NLRP3 Inflammasome in Spinal Cord-Derived Neurons

PPAR-γ Activation Exerts an Anti-inflammatory Effect by Suppressing the NLRP3 Inflammasome in Spinal Cord-Derived Neurons

Comparison of Glaucoma-Relevant Transcriptomic Datasets Identifies Novel Drug Targets for Retinal Ganglion Cell Neuroprotection

Rosiglitazone ameliorates radiation-induced intestinal inflammation in rats by inhibiting NLRP3 inflammasome and TNF-α production

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