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Treatment Effects of Jinlingzi Powder and Its Extractive Components on Gastric Ulcer Induced by Acetic Acid in Rats.
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Jinlingzi powder comprises Melia toosendan Sieb. et Zucc. and Corydalis yanhusuo (Y.H. Chou & Chun C.Hsu) W.T. Wang ex Z.Y. Su & C.Y. Wu and is usually applied in clinic as traditional Chinese medicine for pain. The present study aims to investigate the therapeutic actions of
Therapeutic action of meliacine, a plant-derived antiviral, on HSV-induced ocular disease in mice.
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Ocular herpes simplex virus type-1 (HSV-1) infections remain an important cause of corneal disease which may result in a loss of vision. Meliacine (MA), an antiviral activity present in crude leaf extracts of Melia azedarach L. that inhibits HSV-1 multiplication in vitro, was studied in a murine
Comparison of the Analgesic and Anti-Inflammatory Effects of Xiaoyuningkun Decoction with Cynanchum Paniculatum and Fukeqianjin in a Mouse Model of Pelvic Inflammatory Disease.
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BACKGROUND Preclinical and clinical studies have shown that the extract of Cynanchum paniculatum (bunge) kitag and the fukeqianjin formulation have beneficial effects in pelvic inflammatory disease (PID). This study aimed to compare the effects of Cynanchum paniculatum and fukeqianjin with a new
Intoxication of cattle by the fruits of Melia azedarach.
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Melia azedarach fruits were administered at single doses ranging from 5 to 30 g/kg bw to 10 calves. The animals dosed with 25 g/kg bw and 30 g/ kg bw died, as well as 1/2 cattle that received 15 g/kg bw. Clinical signs were depression, ruminal stasis, anorexia, diarrhea, incoordination, muscle
Cytotoxic and apoptosis-inducing activities of 12-O-Acetylazedarachin B from the fruits of Melia azedarach in human cancer cell lines.
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12-O-Acetylazedarachin B (1), isolated from the fruit extract of Melia azedarach, exhibited potent cytotoxicity against leukemia (HL-60) (IC(50) 0.016 µM) and stomach (AZ521) (IC(50) 0.035 µM) cancer cell lines. Upon assessing the apoptosis-inducing activity in HL-60 cells, compound 1 exhibited
1-O-tigloyl-1-O-deacetyl-nimbolinin B inhibits LPS-stimulated inflammatory responses by suppressing NF-κB and JNK activation in microglia cells.
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Overactivation of microglia may contribute to the pathogenesis of neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, and HIV dementia. Thus, regulating microglial activation has been an important therapeutic strategy for treating neurodegenerative diseases. In this
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