Difference between revisions of "Part:BBa K5332002:Design"

 
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===Design Notes===
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==Background==
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Despite modifications, the inherent cytotoxicity of melittin remains. When applying melittin, introducing amino acid mutations to alter its sequence could further reduce its toxicity to cells, enhancing its safety and applicability without affecting its bioactivity.
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Melittin, as a crucial active component of bee venom, has garnered significant attention in the scientific community for its remarkable anti-inflammatory and immunomodulatory properties. The molecular structure of melittin enables it to effectively intervene in and regulate the human immune response, demonstrating substantial potential in studies of various inflammatory diseases.
  
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In recent years, researchers have gradually unveiled the possible mechanisms of melittin in the treatment of inflammatory bowel disease (IBD) through multiple laboratory studies and animal model experiments. melittin can reduce inflammatory responses by inhibiting the release of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Additionally, it modulates the activity of immune cells, particularly regulatory T cells and macrophages, thereby maintaining balance within the immune system. These mechanisms work synergistically to significantly alleviate intestinal inflammation and aid in restoring normal intestinal function.
  
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In terms of clinical application, melittin shows promise in improving IBD symptoms. However, further research is needed to optimize its safety and efficacy.
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==The anti-inflammatory principle of melittin==
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===Anti-inflammatory effect===
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[[Image:rmelittin1.png|450px|thumb|left|'''Figure 1:'''Anti-inflammatory effect of melittin]]
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Reference: Liu Minchen & Du Ruofei, Chinese Journal of Modern Applied Pharmacy, 2023
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Figure1：
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In terms of anti-inflammatory effects, melittin plays a crucial role in regulating inflammatory signaling pathways. It inhibits the activity of the NF-κB pathway, reducing the expression of inflammatory cytokines such as TNF-α, IL-1β, and IL-6. Melittin can suppress the phosphorylation of IKK and IκB, thereby blocking the nuclear translocation of NF-κB and interfering with inflammatory signal transduction. Additionally, melittin affects the MAPK signaling pathway by inhibiting the phosphorylation of JNK and p38, thus regulating the production of pro-inflammatory cytokines and reducing the activity of inflammatory cells and the secretion of inflammatory mediators. Furthermore, melittin interferes with the JAK/STAT pathway, inhibiting the activity of STAT transcription factors decreasing the secretion of inflammatory cytokines, which helps alleviate inflammatory diseases. Melittin also reduces inflammation by inhibiting Akt phosphorylation, which interferes with the expression of inflammatory proteins and suppresses the production of inflammatory mediators such as COX-2, iNOS, and cPLA2. Additionally, melittin promotes the recruitment of immune cells to the site of inflammation and induces T-cell apoptosis, thereby modulating the immune response and further alleviating inflammation.
  
 
===Source===
 
===Source===

Revision as of 16:43, 30 September 2024


Di-melittin (anti-inflammatory peptide)


Assembly Compatibility:
  • 10
    COMPATIBLE WITH RFC[10]
  • 12
    COMPATIBLE WITH RFC[12]
  • 21
    COMPATIBLE WITH RFC[21]
  • 23
    COMPATIBLE WITH RFC[23]
  • 25
    INCOMPATIBLE WITH RFC[25]
    Illegal NgoMIV site found at 42
  • 1000
    COMPATIBLE WITH RFC[1000]


Background

Melittin, as a crucial active component of bee venom, has garnered significant attention in the scientific community for its remarkable anti-inflammatory and immunomodulatory properties. The molecular structure of melittin enables it to effectively intervene in and regulate the human immune response, demonstrating substantial potential in studies of various inflammatory diseases.

In recent years, researchers have gradually unveiled the possible mechanisms of melittin in the treatment of inflammatory bowel disease (IBD) through multiple laboratory studies and animal model experiments. melittin can reduce inflammatory responses by inhibiting the release of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Additionally, it modulates the activity of immune cells, particularly regulatory T cells and macrophages, thereby maintaining balance within the immune system. These mechanisms work synergistically to significantly alleviate intestinal inflammation and aid in restoring normal intestinal function.

In terms of clinical application, melittin shows promise in improving IBD symptoms. However, further research is needed to optimize its safety and efficacy.

The anti-inflammatory principle of melittin

Anti-inflammatory effect

File:Rmelittin1.png
Figure 1:Anti-inflammatory effect of melittin

Reference: Liu Minchen & Du Ruofei, Chinese Journal of Modern Applied Pharmacy, 2023 Figure1： In terms of anti-inflammatory effects, melittin plays a crucial role in regulating inflammatory signaling pathways. It inhibits the activity of the NF-κB pathway, reducing the expression of inflammatory cytokines such as TNF-α, IL-1β, and IL-6. Melittin can suppress the phosphorylation of IKK and IκB, thereby blocking the nuclear translocation of NF-κB and interfering with inflammatory signal transduction. Additionally, melittin affects the MAPK signaling pathway by inhibiting the phosphorylation of JNK and p38, thus regulating the production of pro-inflammatory cytokines and reducing the activity of inflammatory cells and the secretion of inflammatory mediators. Furthermore, melittin interferes with the JAK/STAT pathway, inhibiting the activity of STAT transcription factors decreasing the secretion of inflammatory cytokines, which helps alleviate inflammatory diseases. Melittin also reduces inflammation by inhibiting Akt phosphorylation, which interferes with the expression of inflammatory proteins and suppresses the production of inflammatory mediators such as COX-2, iNOS, and cPLA2. Additionally, melittin promotes the recruitment of immune cells to the site of inflammation and induces T-cell apoptosis, thereby modulating the immune response and further alleviating inflammation.

Source

The melittin peptide component was synthesized in the laboratory, with its sequence information sourced from the NCBI database.

===References===