The Aloe vera polysaccharides in inflammatory bowel disease: An ethnopharmacological review on the mechanisms of intestinal barrier repair and immunomodulation.
TL;DR
The multi-barrier mechanism of APs, combined with a favorable safety profile, positions APs as a promising adjunctive therapy for IBD, however, the current evidence is predominantly derived from animal models.
Abstract
ETHNOPHARMACOLOGICAL RELEVANCE Aloe vera (Aloe barbadensis Miller) has a medicinal history spanning 1300 years. In traditional Chinese medicine (TCM), Aloe vera is known as "Lu Hui", first recorded in Yao Xing Lun in the Tang Dynasty. Characterized by its bitter taste and cold property, it is attributed to the liver, stomach, and the large intestine meridians, it has been traditionally employed to "clear heat", "purge accumulation and unblock the bowels", and "kill worms". This provides a foundational ethnopharmacological rationale for investigating its therapeutic potential in inflammatory bowel disease (IBD).
Aim
OF THE REVIEW This review systematically evaluates the mechanisms by which Aloe vera polysaccharides (APs) alleviate IBD, with particular emphasis on intestinal barrier integrity, and identifies unresolved questions that hinder clinical translation.
Materials And Methods
A comprehensive literature search was conducted using PubMed, Web of Science, Scopus databases, and other major databases for studies published up to 2026, using keywords including "Aloe vera polysaccharides", "inflammatory bowel disease", "intestinal barrier", and "gut microbiota".
Results
APs demonstrate multi-target efficacy in mitigating IBD pathogenesis through concerted actions on the compromised intestinal barrier system. These actions reinforce the physical barrier by upregulating tight junction proteins and promoting epithelial cell repair, strengthening the chemical barrier by stimulating mucin secretion, modulating the microbial barrier via prebiotic effects that enrich beneficial short-chain fatty acid-producing bacteria, and regulating the immune barrier by rebalancing T-helper cell responses and suppressing key pro-inflammatory pathways (e.g. NF-κB, JAK/STAT). Notably, these synergistic actions collectively reduce oxidative stress, dampen chronic inflammation, and promote mucosal healing.
Conclusion
The multi-barrier mechanism of APs, combined with a favorable safety profile, positions APs as a promising adjunctive therapy for IBD. However, the current evidence is predominantly derived from animal models. Clinical evidence remains extremely limited, comprising only a handful of small-scale studies. Future research should investigate structure-activity relationships, characterize pharmacokinetic profiles, evaluate long-term safety during prolonged administration, and conduct rigorous clinical trials to realize the therapeutic potential of APs for IBD management.