Lotus seeds, also known as Nelumbinis semen, has been utilized for over 7,000 years as vegetable, functional food and medicine. In this study, we primarily investigated the anticancer effects of lotus seed extracts, particularly of the methanolic extract (MELS) on cell proliferation inhibition, apoptosis induction and cell cycle arrest in ovarian cancer cell lines. Further, we studied the phytochemical composition of the MELS by gas chromatography-mass spectrometry (GC-MS) analysis.
View Article and Find Full Text PDFIn this study, we investigated the efficacy of oxymatrine, a phytochemical alkaloid, in reducing inflammation and fibrosis in a rat model of IgA nephropathy (IgAN) through modulation of the TGF-β/SMAD signaling pathway. Thirty Sprague Dawley rats were randomized into control, IgAN, and treatment groups, the latter receiving oxymatrine postinduction of IgAN. Induced by bovine serum albumin, carbon tetrachloride, and lipopolysaccharides, the disease model was validated by immunofluorescence and histopathological analyses, confirming significant renal deposition of IgA and increased fibrosis markers (IL-6, TGF-β, SMAD 3, and α-SMA).
View Article and Find Full Text PDFTraumatic and inherited cataract spiking blindness is caused by accumulated deposition of mutant eye lens protein or lens microarchitecture alteration. A traumatic cataract is a clouding of the eye's natural lens that occurs as a result of physical trauma to the eye. This trauma can be caused by various incidents such as blunt force injury, penetration by a foreign object, or a significant impact on the eye area.
View Article and Find Full Text PDFNeurodegenerative diseases (NDDs) are a collection of incapacitating disorders in which neuroinflammation and neuronal apoptosis are major pathological consequences due to oxidative stress. Neuroinflammation manifests in the impacted cerebral areas as a result of pro-inflammatory cytokines stimulating the Janus Kinase2 (JAK2)/Signal Transducers and Activators of Transcription3 (STAT3) pathway via neuronal cells. The pro-inflammatory cytokines bind to their respective receptor in the neuronal cells and allow activation of JAK2.
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