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Effect of Panax ginseng on preventing acute respiratory tract infection: A protocol for systematic review and meta-analysis.
Zhang, Z, Xu, P, Wang, Z, Zhao, D, Huang, Q, Lu, J, Sun, L, Wang, J, Li, X
Medicine. 2020;(24):e20690
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Abstract
BACKGROUND Acute respiratory tract infection (ARTI) should be deeply concerned all over the world. Panax ginseng (ginseng) as traditional Chinese medicine is widely used in the treatment and health care for respiratory diseases. However, only one similar systematic review based on common cold has been published in 2011. New studies have occurred and a new systematic evaluation which could describe ARTI is needed. METHODS AND ANALYSIS We will search for randomized control trials of ginseng on preventing acute respiratory tract infection in the following 8 databases: Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, AMED (via OVID) and 4 Chinese databases (Chinese Biomedical Literature Database, China National Knowledge Infrastructure, Chinese Science and Technology Periodical Database, and Wan fang Database). The time is limited from the construction of the library to April 2020. The selection of studies, data extraction and quality of assessment will be conducted independently by 2 reviewers. The morbidity of ARTI by assessing self-report, caregiver report or clinical confirmation will be considered as the primary outcome. ARTI-related death among children or adults, other adverse events, absenteeism, laboratory-confirmed infection will be regarded as secondary outcome. All reported side effects and adverse events will be included as safety outcomes. Standard meta-analysis will be performed using Rev Man software V5.3. RESULTS This study will provide a better understanding of the association between P ginseng and ARTI. CONCLUSION This systematic review may offer stronger evidences for the clinicians to prevent the patients from ARTI and update the former one based on basic diseases and the safety. PROSPERO REGISTRATION NUMBER CRD42020181317.
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Green tea extract and (-)-epigallocatechin-3-gallate inhibit hypoxia- and serum-induced HIF-1alpha protein accumulation and VEGF expression in human cervical carcinoma and hepatoma cells.
Zhang, Q, Tang, X, Lu, Q, Zhang, Z, Rao, J, Le, AD
Molecular cancer therapeutics. 2006;(5):1227-38
Abstract
Green tea extract and its major component (-)-epigallocatechin-3-gallate (EGCG) exhibit antiangiogenic activities in various experimental tumor models. A growing body of evidence has established that hypoxia-inducible factor-1alpha (HIF-1alpha) and its downstream target, vascular endothelial growth factor (VEGF), play a critical role in tumor angiogenesis. In this study, we investigated the effect of green tea extract and EGCG on HIF-1alpha and VEGF expression in human cervical carcinoma (HeLa) and hepatoma (HepG2) cells. Our results showed that green tea extract and EGCG significantly inhibited hypoxia- and serum-induced HIF-1alpha protein accumulation in these cancer cells but had no effects on HIF-1alpha mRNA expression. Suppression of HIF-1alpha protein by green tea extract and EGCG also resulted in a drastic decrease in VEGF expression at both mRNA and protein levels. The mechanisms of green tea extract and EGCG inhibition of hypoxia-induced HIF-1alpha protein accumulation seem to involve the blocking of both phosphatidylinositol 3-kinase/Akt and extracellular signal-regulated kinase 1/2 signaling pathways and the enhancing of HIF-1alpha protein degradation through the proteasome system. In addition, green tea extract and EGCG inhibited serum-induced HIF-1alpha protein and VEGF expression by interfering with the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin signaling pathways, which play a crucial role in the protein translational machinery cascade. Functionally, green tea extract and EGCG abolished both chemoattractant- and hypoxia-stimulated HeLa cell migration. Our data suggested that HIF-1alpha/VEGF function as therapeutic target for green tea extract and EGCG in the context of cancer chemoprevention and anticancer therapy.