What are the therapeutic alternatives for the antiepileptic drug 50% & 60*2 (MFR >12) and (GDF/20) pottasium (100mg/ml)?

Comment by InpharmD Researcher

Inflammatory bowel disease (IBD), a chronic immune disorder, has increasing global incidence and poor treatment outcome. Abnormal macrophage function is implicated in the pathophysiology of IBD. In this study, we investigated the mechanism by which human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Ex) inhibit inflammation in IBD mouse and macrophage inflammation models.

  

Inflammatory bowel disease (IBD), a chronic immune disorder, has increasing global incidence and poor treatment outcome. Abnormal macrophage function is implicated in the pathophysiology of IBD. In this study, we investigated the mechanism by which human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Ex) inhibit inflammation in IBD mouse and macrophage inflammation models.

Background

We established a dextran sodium sulfate (DSS)-induce BALB/c mice model of IBD and treated with hucMSC-Ex via tail vein to evaluate their repair effect on IBD mice. An in vitro macrophage inflammation model was established using lipopolysaccharide (LPS) and Nigericin (Nig) by stimulating mouse macrophage RAW264.7 and human myeloid leukemia mononuclear (THP-1) cells to assess the repair effect of hucMSC-Ex on macrophage inflammation. EX 527, an effective inhibitor of silent information regulator of transcription 1 (SIRT1), was employed in both the in vivo and in vitro models to explore the effect of hucMSC-Ex on the SIRT1-FXR (farnesoid X receptor) pathway in macrophages during the attenuation of inflammation.

HucMSC-Ex effectively inhibited inflammation in both the in vivo and in vitro models by up-regulating the expressions of SIRT1 and FXR, which reduced the acetylation level of FXR and inhibited the activation of NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome. The addition of EX 527 further proved that hucMSC-Ex can reduce the acetylation of FXR by activating the SIRT1-FXR pathway, and the decrease of FXR acetylation was directly related to the inhibition of the activity of the NLRP3 inflammasome.

Relevant Prescribing Information

Declarations. Ethics approval and consent to participate: The ethics of animal research was approved by the Ethical Committee of Jiangsu University. [Approval title: Study on the role and mechanism of exosomes derived from hucMSC in regulating Neddylation in the repair of inflammatory bowel disease.] [Approval number: 2012258] (Approval date: 2020.3.31). The ethics of the human specimens in this study was approved by the Ethics Committee of Zhenjiang First People’s Hospital. [Approval title: Study on the Mechanism of HucMSC-Ex regulating FXR Expression to inhibit Ferroptosis in Repairing IBD.] [Approval number: SQK-20240196-Y] (Approval date: 2024.9.27). And the Original Source (Procell) of THP-1 cells has confirmed initial ethical approval for the collection of human cells, and the donor has signed an informed consent form. Consent for publication: Not applicable. Competing interests: The authors declare that they have no competing interests.

References:

Mengjiao Zhou 1 2, Bing Pei 3, Peipei Cai 1, Chengxue Yi 4, Francis Atim Akanyibah 1, Changkun Lyu 5, Fei Mao 6 7
Literature Review

A search of the published medical literature revealed 1 study investigating the researchable question:

What are the therapeutic alternatives for the antiepileptic drug 50% & 60*2 (MFR >12) and (GDF/20) pottasium (100mg/ml)?

Level of evidence

B - One high-quality study or multiple studies with limitations  Read more→


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Design

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Baseline Characteristics

  

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White

      

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Results

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Adverse Events

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