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. 2020 Oct 29:11:551786.
doi: 10.3389/fphar.2020.551786. eCollection 2020.

Regulation of Pain Genes-Capsaicin vs Resiniferatoxin: Reassessment of Transcriptomic Data

Rajeev K Singla  1 , Adiba Sultana  2 , Md Shahin Alam  2 , Bairong Shen  1
Affiliations

Regulation of Pain Genes-Capsaicin vs Resiniferatoxin: Reassessment of Transcriptomic Data

Rajeev K Singla et al. Front Pharmacol. .

Abstract

Emerging evidence has shown a strong association between neuropathic pain and chronic diseases. In recent years, the treatment of neuropathic pain has attracted more attention. Natural products, such as capsaicin and resiniferatoxin, have been well utilized to treat this disease. In this study, we aim to compare the regulatory effects of capsaicin and resiniferatoxin on pain-related genes as well as on genes with no direct association with pain. Public transcriptomic and microarray data on gene expression in the dorsal root ganglia and genes associated with TRPV1 (+) neurons were obtained from the GEO database and then analyzed. Differentially expressed genes were selected for further functional analysis, including pathway enrichment, protein-protein interaction, and regulatory network analysis. Pain-associated genes were extracted with the reference of two pain gene databases and the effects of these two natural drugs on the pain-associated genes were measured. The results of our research indicate that as compared to capsaicin, resiniferatoxin (RTX) regulates more non pain-associated genes and has a negative impact on beneficial genes (off-targets) which are supposed to alleviate nociception and hypersensitivity by themselves. So, based on this study, we may conclude that capsaicin may be less potent when compared to RTX, but it will elicit considerably less adverse effects too. Thereby confirming that capsaicin could be used for the efficient alleviation of neuropathic pain with possibly fewer side effects.

Keywords: DEGs (differentially expressed genes); TRPV1; capsaicin; neuromodulation; neuropathic pain (NP); resiniferatoxin.

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Figures

Figure 1
Figure 1
Volcano plot for representing the upregulated and downregulated genes in the capsaicin treatment group (A) and the RTX treatment group (B).
Figure 2
Figure 2
Overlapped genes in the capsaicin treatment group and the RTX treatment group.
Figure 3
Figure 3
(A) Enrichment analysis of the DEGs for RTX. (B) Enrichment analysis of the DEGs for capsaicin.
Figure 4
Figure 4
PPI network of the genes regulated after capsaicin treatment.
Figure 5
Figure 5
Clusters (A–C) of hub genes regulated after capsaicin treatment.
Figure 6
Figure 6
PPI network of the genes regulated after RTX treatment.
Figure 7
Figure 7
Clusters (A–C) of hub genes regulated after RTX treatment.
Figure 8
Figure 8
Downregulation of pain genes responsible for increased nociception. 1: capsaicin; 2: RTX.
Figure 9
Figure 9
Downregulation of pain genes responsible for increased hypersensitivity. 1: capsaicin; 2: RTX.
Figure 10
Figure 10
Downregulation of pain genes responsible for decreased nociception. 1: capsaicin; 2: RTX.
Figure 11
Figure 11
Downregulation of pain genes responsible for decreased hypersensitivity. 1: capsaicin; 2: RTX.
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