Melittin Capsules

01.The targeted regulatory mechanism of TNF - α.
TNF - α, as the core inflammatory mediator in pro-inflammatory response, its overexpression can cause disorder of the body's inflammatory response, exacerbate tissue damage and inflammatory infiltration. Mellttin can achieve targeted inhibition of TNF - α by regulating the transcriptional activity of the nuclear factor kappa B (NF - κ B) signaling pathway. Specifically, mellttin can bind to key regulatory factors in the NF - κ B signaling pathway, preventing their translocation into the nucleus, thereby downregulating the transcription and expression levels of TNF - α genes and reducing their secretion and release. This regulation is not a simple inhibitory effect, but presents precise dose-dependent regulatory characteristics.

02.Inhibition and extension of IL-6 secretion.
IL-6, as another key pro-inflammatory mediator, works synergistically with TNF - α to promote the occurrence and development of inflammatory responses, and plays an important role in the sustained progression of chronic inflammation. The regulation of IL-6 by this mainly focuses on the cellular secretion level, and can target the inhibition of IL-6 secretion in inflammatory related cells such as synovial fibroblasts and macrophages. Its pathway of action is mainly achieved by inhibiting the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway.

03.Blocking the pathway of prostaglandin synthesis.
Prostaglandins, as important mediators in inflammatory reactions, rely mainly on the catalytic action of cyclooxygenase (COX) in their biosynthesis process. COX-2, as an inducible cyclooxygenase, is highly expressed under inflammatory stimulation, promoting the synthesis of prostaglandins and exacerbating inflammation and tissue pain. Mellttin can specifically antagonize the activity of COX-2 and block the biosynthesis of prostaglandins. Specifically, mellttin can bind to the active site of COX-2, inhibit its catalytic activity, reduce the conversion of arachidonic acid to prostaglandins.

04.The synergistic effect of inflammatory regulation and experimental evidence.
The inhibition of TNF - α and IL-6 by mellttin and the blockade of prostaglandin synthesis do not exist in isolation, but exhibit significant synergistic effects.

The three work together to inhibit the occurrence and development of inflammatory reactions at different stages, forming a complete inflammatory regulatory network.

Bee needle intervention for rheumatoid arthritis.

As a chronic autoimmune inflammatory disease, its core pathology is joint synovitis, cartilage damage, and deformity. Bee needles can accurately deliver mellttin to the affected joints, reducing synovitis and cartilage degradation by inhibiting inflammatory mediators such as TNF - α and IL-6, as well as MMP-1 and MMP-8 activity, alleviating joint redness, swelling, and pain. The efficacy is comparable to traditional anti-inflammatory drugs and has no hormonal side effects. It can also regulate metabolic disorders to improve intervention effectiveness.

Local intervention for dermatitis.

Dermatitis is often associated with local inflammation and immune disorders. Mellttin can be delivered through bee stings or local infiltration, inhibiting the expression of local TNF - α and IL-6 to reduce inflammation infiltration, relieve redness, swelling, and itching, while regulating the skin barrier, promoting cell repair, reducing flaking and dryness, and quickly taking effect. It can also reduce the risk of systemic exposure and reduce recurrence.