The study of Chinese herbal medicinal compound on implantation : in vitro spheroid-endometrium co-culture

2013 ◽  
Author(s):  
Hoi-yan Cheung
Keyword(s):  
Medicinal Compound ◽  
Chinese Herbal ◽  
Herbal Medicinal

scholarly journals Selected Extracts of Chinese Herbal Medicines: Their Effect on NF-κB, PPARαand PPARγand the Respective Bioactive Compounds

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
E. Rozema ◽  
A. G. Atanasov ◽  
N. Fakhrudin ◽  
J. Singhuber ◽  
U. Namduang ◽  
...  
Keyword(s):  
Herbal Medicines ◽  
Peroxisome Proliferator ◽  
Nuclear Factor ◽  
Albizia Julibrissin ◽  
Chinese Herbal ◽  
Bioassay Guided Fractionation ◽  
Ppar Agonists ◽  
Herbal Medicinal ◽  
Peroxisome Proliferator Activated Receptors

Chinese herbal medicinal (CHM) extracts from fourteen plants were investigated in cell-basedin vitroassays for their effect on nuclear factorκB (NF-κB), a key regulator of inflammation, as well as on peroxisome proliferator-activated receptors (PPARs) being key regulators of genes involved in lipid and glucose metabolism. 43% of the investigated CHMs showed NF-κB inhibitory and 50% PPARαand PPARγactivating effects. Apolar extracts from cortex and flos ofAlbizia julibrissinDurazz. and processed rhizomes ofArisaemasp. andPinellia ternata(Thunb.) Breit. that effectively inhibited TNF-α-induced NF-κB activation and dose-dependently activated PPARαand PPARγwere further investigated. Bioassay-guided fractionation and analysis by GC-MS led to the identification of fatty acids as PPAR agonists, including linoleic and palmitic acid.

Inhibitory effects of Chinese herbal formula Bingdeling on four common bacteria in vitro

2010 ◽  
Vol 30 (2) ◽  
pp. 212-214
Author(s):  
Hong QIAN ◽  
Nong XIAO ◽  
Zhi-feng QIN ◽  
Yan-jun LIU ◽  
Yi-jun SHEN ◽  
...  
Keyword(s):  
Herbal Formula ◽  
Inhibitory Effects ◽  
Chinese Herbal Formula ◽  
Chinese Herbal

scholarly journals The Study on Chinese Herbal Medicinal Prescription with Enzyme Inhibitory Activity. III. The Study of Mao-to with Adenosine 3', 5'-Cyclic Monophosphate Phosphodiesterase

1990 ◽  
Vol 110 (7) ◽  
pp. 504-508 ◽  
Author(s):  
Tamotsu NIKAIDO ◽  
Taichi OHMOTO ◽  
Takashi KUGE ◽  
Akiko YANAGISAWA ◽  
Kiyomi TEINOZAWA ◽  
...  
Keyword(s):  
Inhibitory Activity ◽  
Cyclic Monophosphate ◽  
Chinese Herbal ◽  
Herbal Medicinal

scholarly journals Chinese Herbal Preparation SaiLuoTong Alleviates Brain Ischemia via Nrf2 Antioxidation Pathway–Dependent Cerebral Microvascular Protection

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiao-Di Fan ◽  
Ming-Jiang Yao ◽  
Bin Yang ◽  
Xiao Han ◽  
Ye-Hao Zhang ◽  
...  
Keyword(s):  
Brain Ischemia ◽  
Statistical Significance ◽  
Therapeutic Effects ◽  
Herbal Preparation ◽  
Model Group ◽  
Sod Activity ◽  
Nrf2 Pathway ◽  
Chinese Herbal ◽  
Therapeutic Mechanism

Stroke is one of the most devastating diseases worldwide. The Chinese herbal preparation SaiLuoTong (SLT) capsule showed outstanding therapeutic effects on stroke and its sequelae. The aim of this study was to further elucidate its therapeutic mechanism. We duplicated a permanent cerebral ischemia model in rats by MCAO and used SLT (33 and 16.5 mg/kg) to intervene. The results showed SLT dose dependently decreased infarction volumes, relieved neuron degeneration and loss, and ameliorated neurological functions, and the dose of 33 mg/kg had statistical significance (compared with the model group, p < 0.05); SLT of 33 mg/kg also significantly inhibited the elevation in brain water content and the loss in claudin-1 and occludin expressions; additionally, it significantly increased nucleus translocation of Nrf2, elevated the expression of HO-1, and raised the activity of SOD and content of GSH (compared with the model group, p < 0.05 or 0.01). These results testified SLT’s anti-brain ischemia effect and hint this effect may be related to the protection of brain microvascular endothelial cells (BMECs) that is dependent on the Nrf2 pathway. To further testify, we cultured hCMEC/D3 cells, duplicated OGD/R model to simulate ischemia, and used SLT (3.125, 6.25, and 12.5 mg/L) to treat. SLT dose dependently and significantly inhibited the drop in cell viabilities, and activated the Nrf2 pathway by facilitating Nrf2 nucleus translocation, and increasing HO-1 expression, SOD activity, and GSH content (compared with the model group, p < 0.05 or 0.01); last, the anti-OGD/R effects of SLT, including raising cell viabilities, inhibiting the elevation in dextran permeability, and preserving expressions of claudin-1 and occludin, were all abolished by Nrf2 siRNA interference. The in vitro experiment undoubtedly confirmed the direct protective effect of SLT on BMECs and the obligatory role of the Nrf2 pathway in it. Collectively, data of this study suggest that SLT’s therapeutic effect on brain ischemia is related to its Nrf2-dependent BMECs protection.

scholarly journals Shenshuaikang Enema, a Chinese Herbal Remedy, Inhibited Hypoxia and Reoxygenation-Induced Apoptosis in Renal Tubular Epithelial Cells by Inhibiting Oxidative Damage-Dependent JNK/Caspase-3 Signaling Pathways Using Network Pharmacology

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Hongmei Lu ◽  
Xinyi Luo ◽  
Yuhua He ◽  
Bo Qu ◽  
Liangbin Zhao ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Caspase 3 ◽  
Cell Counting ◽  
Network Pharmacology ◽  
In Vitro Experiments ◽  
Chinese Herbal ◽  
Cell Vitality ◽  
Target Network ◽  
Renal Tubular

Background. Acute kidney injury (AKI) is a common clinically critical illness with serious consequences for the patients. Shenshuaikang enema (SE) is a Chinese herbal compound that is used to treat AKI in clinical practice. However, its mechanism of action remains unclear. Aim. The aim of this study was to investigate the therapeutic effect of SE and explore the molecular mechanisms using network pharmacology and in vitro experiments. Materials and Methods. The herb-component-target network was constructed based on network pharmacology. The predicted targets and pathways were validated using in vitro experiments. A renal tubular epithelial cell line (HK-2 cells) was exposed to hypoxia and reoxygenation (H/R) using air-tight conditions for five hours and treated with different concentrations of SE (25%, 50%, and 75%) to assess cell viability and apoptosis and determine the optimal experimental dose. Subsequently, H/R-injured HK-2 cells were pretreated with the optimal SE dose and then randomly divided into three groups, the SE, SE-SP600125 (inhibitor of JNK), and SE-NAC (antioxidant) groups. The cell vitality, apoptosis, and death were evaluated using the cell counting kit 8 (CCK8) and carboxyfluorescein succinimidyl ester/propidium iodide (CFSF/PI) staining. The apoptosis-related protein JNK and Caspase-3 were assessed by Western blot. Expression of JNK and Caspase-3 genes was analyzed using real-time quantitative polymerase chain reaction (RT-qPCR). Results. 123 active components and 226 targets were identified from four herbs that composed the herb-compound-target network based on transcriptomics and network pharmacology analyses. The KEGG pathway analyses revealed that the mitochondrial apoptosis pathway was involved in the therapeutic AKI effects of SE. Cell vitality of H/R-induced HK-2 cells was obviously increased when treating them with SE, and the apoptosis was significantly inhibited, especially in the SE (50%) group at 4 and 12 h after modeling. Pretreatment with antioxidant NAC obviously prevented cell death compared to the SE (50%) group, while no obvious reduction of apoptosis was observed in the SP600125 group. JNK expression level was significantly increased in the SE (50%) group compared to the SP600125 ( P < 0.01 ) and the NAC group ( P < 0.05 ). Caspase-3 was downregulated in the SE (50%) group compared to the SP600125 ( P < 0.01 ) and NAC group ( P < 0.05 ). Caspase-3 activation in the SP600125 group was higher than that in the NAC group ( P < 0.05 ). Moreover, the oxidative damage-dependent JNK/Caspase-3 pathway was identified in the H/R-injured HK-2 cells by inhibiting the JNK activation and oxidative damage. Conclusions. Our findings suggested that the H/R-triggered apoptosis in HK-2 cells was abrogated by SE by upregulating the oxidative damage-dependent JNK to trigger suppression of Caspase-3.

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