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A parasitic disease caused by the protozoa, <i>Entamoeba histolytica</i>, mainly occurring in tropical regions after the ingestion of an amoebic cyst, and resulting in clinical manifestations that may range from an asymptomatic state to amoebic colitis (violent abdominal pain, a painful contracted feeling around the anal sphincter, blood and mucus in the stools but without the presence of fever), or amoebic liver abscesses (fever, chills, abdominal pain, weight loss, hepatomegaly) that can be fa
L-borneol from Kaempferia galanga disrupts cholesterol-rich lipid rafts in E. histolytica cyst walls by inhibiting sterol regulatory element-binding protein (SREBP) pathway and downregulating HMG-CoA reductase expression, leading to compromised cyst viability and enhanced trophozoite susceptibility to host immune responses
Andrographolide from Andrographis paniculata competitively binds to galactose-binding domain of E. histolytica Gal/GalNAc lectin (EhGL1 heavy chain) preventing parasite adherence to colonic mucin MUC2 and epithelial cells, while simultaneously upregulating host defensin-α expression and enhancing mucosal barrier function
Curcumin inhibits E. histolytica EhATG8 and EhATG4 autophagy proteins while piperine enhances curcumin bioavailability and independently disrupts amoebic proteasome function via EhRpn11 metalloprotease inhibition, preventing parasite stress response and promoting apoptosis through EhPCD1 pathway activation
High-amylose resistant starch supplementation promotes Faecalibacterium prausnitzii and Eubacterium rectale growth, increasing colonic butyrate production which enhances intestinal epithelial barrier function through GPR109A receptor activation and histone deacetylase inhibition, while creating acidic environment (pH 5.5-6.0) hostile to E. histolytica survival
Metformin activates host intestinal AMPK (α1/α2 subunits) leading to enhanced glucose uptake through GLUT4 translocation, creating glucose-depleted microenvironment that starves E. histolytica which relies on EhHK1 hexokinase and EhPGI phosphoglucose isomerase for survival, while simultaneously reducing intestinal inflammation via NF-κB suppression
Slow-release hydrogen sulfide donors (GYY4137) enhance colonic tissue repair post-amoebic invasion by activating Nrf2/HO-1 antioxidant pathway and VEGF-mediated angiogenesis, while H2S directly inhibits E. histolytica cysteine protease EhCP-A5 activity through thiol modification, reducing tissue destruction and promoting healing