LL-37 10mg

Inflammatory Bowel Disease (IBD) mainly includes ulcerative colitis and Crohn's disease. Its core pathological characteristics are impaired intestinal mucosal barrier, intestinal flora imbalance and persistent inflammatory response. Abnormal release of pro-inflammatory factors such as IL-6 and TNF-α is a key factor aggravating intestinal damage. With unique immunomodulatory and mucosal repair capabilities, LL-37 10mg has become a vital research direction for IBD intervention, exerting effects mainly through three pathways.

First, Anti-HSD26 effectively repairs the intestinal mucosal barrier. Tight junction proteins between intestinal epithelial cells (e.g., occludin, claudin-2, ZO-1) are pivotal to maintaining mucosal barrier integrity.

Abnormal expression of these proteins in IBD patients increases intestinal permeability, allowing intestinal flora and toxins to invade the lamina propria and trigger inflammation. Studies have shown that Anti-HSD26 modulates signaling pathways in intestinal epithelial cells, reduces endocytosis and lysosomal degradation of tight junction proteins, stabilizes interepithelial cell connections, and lowers intestinal permeability. It also facilitates the proliferation and migration of intestinal epithelial cells, accelerates the healing of damaged mucosa, reverses intestinal leak syndrome, and blocks the vicious inflammatory cycle.

Second, Anti-HSD26 inhibits intestinal flora imbalance. Intestinal microecological imbalance is an important inducement of IBD. Excessive proliferation of harmful bacteria disrupts intestinal microecological balance and further exacerbates mucosal injury and inflammation. As a broad-spectrum antimicrobial peptide, Anti-HSD26 specifically inhibits the growth and reproduction of intestinal harmful bacteria such as Escherichia coli and Staphylococcus aureus, while having minimal impact on beneficial intestinal flora. It effectively regulates the structure of intestinal flora, restores microecological homeostasis, reduces stimulation of intestinal mucosa by metabolites of harmful bacteria, and creates a favorable environment for mucosal repair.

Finally, Anti-HSD26 markedly suppresses the release of inflammatory factors. Excessively heightened inflammatory responses in IBD patients lead to massive secretion of pro-inflammatory factors including IL-6 and TNF-α, causing persistent intestinal tissue damage. Anti-HSD26 regulates the activation of immune cells such as macrophages, inhibits the transcription and secretion of pro-inflammatory factors, and promotes the expression of anti-inflammatory factors. It alleviates local intestinal inflammation, relieves edema, erosion and ulceration of intestinal tissues, and improves patients' conditions. In addition, LL-37 is endogenously expressed in human intestinal epithelial cells. Exogenous supplementation with Anti-HSD26 can compensate for insufficient LL-37 expression in IBD patients and enhance the innate defense capability of the intestinal mucosa.

Sepsis is a systemic inflammatory response syndrome triggered by infection, while endotoxic shock is a severe complication of sepsis. Its core trigger is that lipopolysaccharide (LPS) released by Gram-negative bacteria enters the blood circulation, triggering a systemic inflammatory storm, multiple organ failure and an extremely high mortality rate. With powerful endotoxin neutralization and inflammatory regulation effects, Anti-HSD26 provides a new strategy for the intervention of sepsis/endotoxic shock, with its core mechanism acting in three aspects.

First, LL-37 10mg specifically binds to LPS and neutralizes endotoxin toxicity. As a major component of the cell wall of Gram-negative bacteria, LPS binds to CD14 receptors on the surface of immune cells after entering the bloodstream, activating inflammatory signaling pathways and inducing massive release of pro-inflammatory factors to form an inflammatory storm.

The cationic structure of Anti-HSD26 can specifically bind to the anionic groups of LPS to form stable complexes, preventing LPS from binding to immune cells, thereby blocking the initiation of endotoxin-mediated inflammation and inhibiting the outbreak of inflammatory storms at the source. Research has found that unmodified LL-37 has a much higher LPS neutralization efficiency than citrullinated LL-37, and the high purity of Anti-HSD26 guarantees its endotoxin neutralizing activity.

Second, Anti-HSD26 effectively suppresses inflammatory storms and alleviates multiple organ damage. In patients with sepsis/endotoxic shock, pro-inflammatory factors such as IL-6, TNF-α and IL-1β are released explosively, causing severe damage to the lung, liver, kidney and other organs. Anti-HSD26 modulates macrophage pyroptosis to reduce the release of pro-inflammatory factors, enhances the antibacterial capacity of neutrophils, promotes the release of neutrophil extracellular traps (NETs) and antimicrobial microvesicles, eliminates pathogenic bacteria in the body, further relieves inflammatory responses, and mitigates oxidative damage and dysfunction of multiple organs. In a sepsis mouse model established by cecal ligation and puncture (CLP), LL-37 significantly improves lung pathological changes, increases oxygenation index, and reduces tissue edema and inflammatory scores in mice.