noscapine and Kidney-Diseases

noscapine has been researched along with Kidney-Diseases* in 3 studies

Reviews

1 review(s) available for noscapine and Kidney-Diseases

ArticleYear
NSAIDS for renal and biliary colic: intramuscular diclofenac.
    Drug and therapeutics bulletin, 1987, Nov-02, Volume: 25, Issue:22

    Topics: Anti-Inflammatory Agents, Non-Steroidal; Biliary Tract Diseases; Codeine; Colic; Diclofenac; Drug Combinations; Humans; Injections, Intramuscular; Kidney Diseases; Morphine; Noscapine; Papaverine; Scopolamine Derivatives

1987

Trials

1 trial(s) available for noscapine and Kidney-Diseases

ArticleYear
Prostaglandin-synthetase inhibition with diclofenac sodium in treatment of renal colic: comparison with use of a narcotic analgesic.
    Lancet (London, England), 1982, May-15, Volume: 1, Issue:8281

    Topics: Adolescent; Adult; Aged; Analgesics, Opioid; Codeine; Colic; Cyclooxygenase Inhibitors; Diclofenac; Double-Blind Method; Drug Combinations; Female; Humans; Injections, Intramuscular; Kidney Diseases; Male; Middle Aged; Morphine; Noscapine; Papaverine; Phenylacetates; Random Allocation; Scopolamine Derivatives

1982

Other Studies

1 other study(ies) available for noscapine and Kidney-Diseases

ArticleYear
Noscapine alleviates unilateral ureteral obstruction-induced inflammation and fibrosis by regulating the TGFβ1/Smads signaling pathways.
    Biochimica et biophysica acta. Molecular cell research, 2024, Volume: 1871, Issue:1

    Renal fibrosis is a common pathway leading to progressive renal function loss in various forms of chronic kidney disease. Many fibrogenic factors regulate renal fibrosis; two key players are post-injury inflammation and transforming growth factor-β1 (TGF-β1)-induced myofibroblast differentiation. Myofibroblast differentiation is tightly regulated by the microtubule polymerization. Noscapine, an antitussive plant alkaloid, is a potent microtubule-interfering agent previously identified as a potential anticancer compound. Here, we examined how noscapine affects renal fibrogenesis in an in vitro renal fibroblast model and an in vivo unilateral ureteral obstruction (UUO) model. UUO mice were intraperitoneally treated with noscapine at 1 day before UUO surgery and daily thereafter. At 7 days post-surgery, kidneys were collected for further analysis. To analyze whether noscapine inhibits downstream TGF-β1-related signaling, we pre-incubated NRK-49F fibroblasts with noscapine and then performed TGF-β1 stimulation. In UUO mice, noscapine attenuated extracellular matrix protein deposition and the expression levels of type I collagen, type IV collagen, α-smooth muscle actin, and fibronectin. In addition, noscapine decreased tubulointerstitial inflammation in UUO kidneys by reducing TLR2 expression, modulating NLRP3 inflammasome activation, reducing macrophage infiltration, and antagonizing the M2 macrophage phenotype. Furthermore, noscapine pre-incubation suppressed the TGF-β1-induced fibroblast-myofibroblast transformation by downregulating the TGF-β/Smads signaling pathways in NRK-49F cells. These results suggest that noscapine reduces tubulointerstitial inflammation and fibrosis in the kidneys of UUO mice and inhibits the fibroblast-myofibroblast transformation induced by TGF-β1. Noscapine is an over-the-counter antitussive that has been used safely for several decades. Therefore, noscapine is an attractive therapeutic agent for inhibiting renal tubulointerstitial fibrosis.

    Topics: Animals; Antitussive Agents; Fibrosis; Inflammation; Kidney Diseases; Mice; Noscapine; Signal Transduction; Transforming Growth Factor beta1; Ureteral Obstruction

2024