|CFN99505||Aristolochic acid A
1. Aristolochic acid A is a potent nephrotoxin.
2. Aristolochic acid A strongly induces toxic damage during ovarian maturation by inhibiting Akt phosphorylation-mediated suppression of apoptosis.
1. Colchicine prevents amyloidosis in our high-risk population and that it can prevent additional deterioration of renal function in patients with amyloidosis who have proteinuria but not the nephrotic syndrome.
2. Colchicine binds at a location where it prevents curved tubulin from adopting a straight structure, which inhibits assembly, and microtubules are cytoskeletal polymers of tubulin involved in many cellular functions.
3. Colchicine has anti-mitotic activity, it interacts with tubulin and perturbs the assembly dynamics of microtubules; though its use has been limited because of its toxicity, colchicine can still be used as a lead compound for the generation of potent anti-cancer drugs.
4. Colchicine can treat familial mediterranean fever.
5. Colchicine may exert its prophylactic effects on cytokine-provoked inflammation by diminishing the qualitative expression of E-selectin on endothelium, and its therapeutic effects by diminishing the quantitative expression of L-selectin on neutrophils.
1. Norcantharidin inhibits the canonical Wnt signal pathway in NSCLC, by activating WIF-1 via promoter demethylation.
2. Norcantharidin could be an effective agent for targeting neo-lymphangiogenesis to inhibit lymphangiogenesis, by downregulating the expression of VEGF-C and VEGF-D.
3. Norcantharidin enhances TIMP‑2 antitumor and anti‑VM activities in GBCs through downregulating MMP‑2 and MT1‑MMP.
1. Strictosamide may have important effects on inflammation and inflammatory pain.
2. Strictosamide is slightly toxic to Charles River mouse (LD(50)=723.17 mg/kg), producing CNS depression and kidney toxicity.
3. Strictosamide has nonsignificant in vitro and in vivo effect on kidney Na(+),K(+)-ATPase activity but produced an in vivo increase of Na(+),K(+)-ATPase activity of brain.
1. Telocinobufagin is the major endogenous digitalis-like factor.
2. Telocinobufagin significantly decreases the bacterial burdens in the spleen and prolongs the survival time of FIST-immunized mice challenged with live S. typhimurium.
3. Telocinobufagin has immunomodulatory activity, can enhance a Th1 immune response to control intracellular infections, could be developed as a novel immunotherapeutic agent to treat cancer and other immune-mediated diseases.