The American journal of Chinese medicine
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Qu-Yu-Jie-Du decoction (QYJD) is a commercially available traditional Chinese medicine (TCM). It is an aqueous extract of a Chinese herbal formula primarily consisting of eight TCM herbs: Taraxacum campylodes G. E. Haglund, Coix lacryma-jobi L., Smilax glabra Roxb., Sanguisorba officinalis L, Styphnolobium japonicum (L.) Schott, Prunus persica (L.) Batsch, Sophora flavescens Aiton, and Eupolyphaga sinensis Walker. ⋯ Elevated Nrf2 and HO-1 mRNA levels were also observed in QYJD-treated mice. These findings showed that QYJD could elicit anti-inflammatory and anti-oxidative stress response in vitro in a cell line and in vivo in a DSS-induced colitis mouse model. These responses may contribute to the overall anticolon cancer effect of QYJD.
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Amyloid [Formula: see text] (A[Formula: see text]) plays a major role in the pathogenesis of Alzheimer's disease (AD). The accumulation of misfolded A[Formula: see text] causes oxidative and inflammatory damage leading to apoptotic cell death. Chinese herbal medicine (CHM) has been widely used in clinical practice to treat neurodegenerative diseases associated with oxidative stress and neuroinflammation. ⋯ Our results showed that G. inflata extract and its two constituents displayed potentials of A[Formula: see text] aggregation inhibition and radical-scavenging in biochemical assays, A[Formula: see text] misfolding inhibition and reactive oxygen species (ROS) reduction in A[Formula: see text]-GFP 293 cells, as well as neurite outgrowth promotion, acetylcholinesterase inhibition and SOD2 up-regulation in A[Formula: see text]-GFP SH-SY5Y cells. Meanwhile, both G. inflata extract and its constituents suppressed NO, TNF-[Formula: see text], IL-1[Formula: see text], PGE2 and/or Iba1 productions in inflammation-stimulated RAW 264.7 or BV-2 cells. G. inflata extract and its constituents further protected A[Formula: see text]-GFP SH-SY5Y cells from BV-2 CM-induced cell death by ameliorating reduced BCL2 and attenuating increased IGFBP2, cleaved CASP3, BAD and BAX. Collectively, G. inflata extract, licochalcone A and liquiritigenin display neuroprotection through exerting anti-oxidative and anti-inflammatory activities to suppress neuronal apoptosis.
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Diabetic retinopathy (DR), one of the most common microvascular complications of diabetic mellitus, is currently the main cause of adult-acquired blindness. The pathogenesis of DR is complex and the current clinical application of various treatment methods cannot completely prevent the development of this disease. Many reports have been published regarding the treatment of DR with Traditional Chinese Medicine (TCM), which has received increasing attention from medical practitioners worldwide. ⋯ Thereafter, the status quo of DR treatment using TCM had been summarized according to four aspects - compound formula therapy, Chinese herbal medicine extracts and monomer therapy, integrated traditional Chinese and Western medicine therapy, and Chinese medicine external treatment. According to the literature reviewed herein, TCM has had definite effects on the prevention and treatment of DR, especially when used in combination with modern medical methods. However, the lack of a unified standard on the syndrome differentiation of DR and the lack of support of evidence-based medicine theory in clinical practice have been consistent concerns in previous research studies and needs to be addressed in subsequent studies.
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The cytokine C-X-C motif chemokine ligand 8 (CXCL8) is produced in the tumor microenvironment and has an important role in cancer pathogenesis. CXCL8 activates the nuclear factor (NF)-[Formula: see text]B signaling. However, the role of NF-[Formula: see text]B inactivation in apoptosis induced by negative regulation of CXCL8 remains unclear. ⋯ When Akt was silenced, MRGX treatment of HepG2 cells overexpressing CXCL8 decreased nuclear translocation of NF-[Formula: see text]B, whereas Akt overexpression increased nuclear translocation of NF-[Formula: see text]B in MRGX-treated HepG2 cells. Moreover, MRGX negatively regulated the TNF-[Formula: see text]-mediated I[Formula: see text]B/NF-[Formula: see text]B pathway to promote Bax activation, resulting in caspase-3 activation and apoptosis. Taken together, these results indicated that MRGX inhibited CXCL8-mediated Akt/NF-[Formula: see text]B signaling, which upregulated Bax activation and consequently induced apoptosis in HepG2 cells.
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Puerarin is a traditional Chinese medicine with beneficial effects of reduced depression-like behaviors in mice with stress. Previous studies also show that puerarin can produce neuroprotective effect via activating the Akt or increased brain-derived neurotrophic factor (BDNF) expression. Interestingly, BDNF and Akt downstream target, mammalian target of rapamycin (mTOR) mediate the fast-acting antidepressant properties of ketamine. ⋯ Moreover, a significant increase in the GluR1 phosphorylation at its PKA site was noted following puerarin treatment. Our findings are the first to demonstrate that the antidepressant-like actions of puerarin require AMPAR-mTOR signaling pathway activation, are associated with an increased BDNF level and facilitate AMPAR membrane insertion. These findings provide preclinical evidence that puerarin may possess antidepressant property which is mediated by the glutamatergic system.