Assessment of the Anti-Inflammatory Effects of Centella asiatica in Modulating Neurogenic Pathways Associated with Pruritus

Chronic pruritus represents a complex neuroimmune disorder characterized by the persistent activation of cutaneous sensory neurons and dysregulated immune signaling. Hyperactivation of transient receptor potential (TRP) channels, including TRPV۱ and TRPA۱, alongside elevated levels of pruritogenic neuropeptides such as substance P (SP) and calcitonin gene-related peptide (CGRP), drives neurogenic inflammation and sustains peripheral and central itch circuits. Concurrently, pro-inflammatory cytokines, including IL-۳۱, IL-۶, and TNF-α, released by keratinocytes, mast cells, and infiltrating immune cells, exacerbate neuronal sensitization and perpetuate chronic itch. Centella asiatica, a medicinal plant rich in pentacyclic triterpenoids such as asiaticoside, madecassoside, and their aglycones, exhibits potent anti-inflammatory, antioxidant, and neuroprotective properties. Preclinical and emerging clinical evidence indicates that C. asiatica modulates pruritogenic pathways through multiple mechanisms: (i) suppression of pro-inflammatory cytokine production, (ii) inhibition of sensory neuron hyperexcitability, (iii) regulation of TRP channel activity, and (iv) attenuation of neuropeptide-mediated cutaneous sensitization. Collectively, these dual anti-inflammatory and neurogenic modulatory effects position C. asiatica as a promising candidate for the development of targeted therapeutics for chronic inflammatory and neuropathic itch. Elucidation of these molecular and cellular pathways provides a rationale for optimized topical or systemic interventions, with potential to reduce reliance on corticosteroids and systemic anti-pruritic agents, while minimizing adverse effects.

کلیدواژه ها:

Centella asiatica ، neurogenic pruritus ، TRPV۱/TRPA۱ modulation ، neuroimmune crosstalk ، anti-inflammatory phytotherapy