cecal

1. Tussilagone inhibits dendritic cell function through the induction of heme oxygenase-1. 2. Tussilagone has anti-cancer activity, might be a potential chemotherapeutic agent for the prevention and treatment of human colon cancer. 3. Tussilagone has anti

Demethoxyencecalin is extracted from Helianthus annuus with antifungal activities.

Encecalinol, a compound isolated from the aerial parts of Ageratina grandifolia, acts as a potent inhibitor of calmodulin [1].

(S)-O-Methylencecalinol (compound 10), a calmodulin-targeting molecule, has been isolated from the aerial parts of *Ageratina grandifolia* [1].

Encecalin and demethylencecalin are major phytotoxic compounds isolated from Helianthella quinquenervis (Hook) A Gray (Asteraceae), they inhibit photosystem II (from water to 2,5-dibromo-3-methyl-6-isopropyl-1,4 p-benzo-quinone).They retard seed germinati

Demethoxyencecalinol is a natural product for research related to life sciences. The catalog number is TN5686 and the CAS number is 71822-00-9.

Demethylisoencecalin (6-Acetyl-5-hydroxy-2,2-dimethyl-2H-1-benzopyran) has anti-hyperglycemic activity.

SIRT5 inhibitor 7 (compound 58), a substrate-competitive and selective SIRT5 inhibitor with IC 50 = 310 nM, significantly attenuated renal dysfunction and pathological damage in lipopolysaccharide (LPS)- and cecum ligation/perforation (CLP)-induced septic AKI mice, and modulated proteinsuccinimidylation and proinflammatory cytokine release and pro-inflammatory cytokine release in the kidneys of acute kidney injury (AKI) mice.

Ferroptosis-IN-12 (Cpd-A1) is an inhibitor of ferroptosis. It effectively suppresses ferroptosis in mouse renal tubular epithelial cells (mTECs) treated with Erastin and improves renal function in dose-dependent manners in mouse models of acute kidney injury (AKI) induced by ischemia/reperfusion (I/R) or cecal ligation and puncture (CLP). This compound also reduces renal tubular damage and eliminates inflammation. Exhibiting good plasma stability and high distribution in renal tissues during pharmacokinetic studies in mice, Ferroptosis-IN-12 shows promising potential for research in the field of AKI.

Urobilinogens comprise a mixture of bilirubin metabolites, including D-urobilinogen, L-urobilinogen (stercobilinogen), and i-urobilinogen (mesobilirubinogen). These compounds are produced from bilirubin by gut microbiota. In mice on a high-fat diet, the cecal concentrations of D-urobilinogen, L-urobilinogen, and i-urobilinogen are increased. Furthermore, elevated fecal levels of L-urobilinogen are inversely associated with reduced blood hemoglobin levels in patients with heterozygous β-thalassemia.

AM 281, a cannabinoid antagonist, reduces neurologic dysfunction and mortality rate after cecal ligation and puncture in rats.

LL-37 is a cationic and α-helical antimicrobial peptide expressed in human bone marrow, testis, granulocytes, and gingival epithelium and is upregulated in psoriatic lesions. It inhibits growth of Gram-positive E. coli D21 and Gram-negative B. megatarium in a concentration-dependent manner and LL-37 expression is induced in A549 epithelial cells, alveolar macrophages, neutrophils, and monocyte-derived macrophages following M. tuberculosis infection. LL-37 binds sheep erythrocytes coated with S. minnesota Re-LPS and induces agglutination with a minimal agglutinating concentration (MAC) of 12.1 μg/ml. It is a chemoattractant for, and can induce calcium mobilization in, human monocytes, neutrophils, and T cells that naturally express formyl peptide receptor-like 1 (FPRL1) and FPRL1-transfected HEK293 cells. LL-37 (10-15 μM) pretreatment of dengue virus type 2 (DENV-2) reduces its infectivity as well as levels of viral genomic RNA and NS1 antigen. In vivo, LL-37 inhibits cecal ligation and puncture-induced caspase-1 activation and pyroptosis of peritoneal macrophages, reduces levels of the inflammatory cytokines IL-1β, IL-6, and TNF-α, and improves survival in polybacterial septic mice.

UFP101 is a synthetic peptide that functions as an antagonist of the nociceptin receptor, demonstrating high affinity with a Ki of 0.06 nM in CHO cells expressing the human receptor. It exhibits selectivity for the nociceptin receptor over the κ-opioid receptor, with a Ki of 204 nM in CHO cells expressing the rat receptor. The compound effectively inhibits GTPγS release from the nociceptin receptor in CHO cell membranes, with an EC50 of 1.86 nM. When administered intracerebroventricularly at a dose of 10 nmol/animal, UFP101 prolongs the latency to tail withdrawal in the tail-flick test in mice, indicating its potential as an analgesic. Additionally, at doses of 0.003, 0.03, and 0.3 mg/kg, UFP101 enhances survival in a sepsis mouse model induced by cecal ligation and puncture, suggesting potential therapeutic applications in sepsis management.

CKG012 is an inhibitor of the Wnt/β-catenin signaling pathway that inhibits the release of HMGB1 and the transcription of β-catenin. It exhibits attenuating activities against cecal ligation and puncture (CLP)-induced sepsis and multiple myeloma cancer [1] [2].

The impact of spleen tyrosine kinase (Syk) signaling might be prominent in lupus because (i) Syk is a shared downstream signaling molecule among circulating immune complex, LPS, and (1→3)-β-D-glucan (BG), and (ii) all of these factors are detectable in the serum of Fc gamma receptor IIb-deficient (FcgRIIb-/-) mice with sepsis. Syk inhibition downregulated several inflammatory pathways in FcgRIIb-/- macrophages activated with BG + LPS suggesting the potential anti-inflammatory impact of Syk inhibitors in lupus. Indeed, administration of a Syk inhibitor prior to cecal ligation and puncture (CLP) sepsis in FcgRIIb-/- mice reduced baseline lupus-induced proinflammatory cytokines and attenuated sepsis severity as evaluated by mortality, organ injury, serum LPS, and post-sepsis serum cytokines.