Estrogen receptor beta (ERβ) is one of the two key receptors (ERα, ERβ) that facilitate biological actions of 17β-estradiol (E2). ERβ is widely expressed in many tissues, and its expression is reduced or lost during progression of many tumors. ERβ facilitates estrogen signaling by both genomic (classical and non-classical) and extra-nuclear signaling. Emerging evidence suggests that ERβ functions as a tissue-specific tumor suppressor with anti-proliferative actions. Recent studies have identified a number of naturally available selective ERβ agonists. Targeting ERβ using its naturally available ligands is an attractive approach for treating and preventing cancers. This review presents the beneficial actions of ERβ signaling and clinical utility of several natural ERβ ligands as potential cancer therapy.
Antineoplastic Agents, Phytogenic ; pharmacology ; therapeutic use ; Equol ; pharmacology ; therapeutic use ; Estrogen Receptor beta ; antagonists & inhibitors ; metabolism ; Flavanones ; pharmacology ; therapeutic use ; Genistein ; pharmacology ; therapeutic use ; Glycyrrhiza ; chemistry ; Humans ; Ligands ; Neoplasms ; drug therapy ; metabolism ; Phytotherapy ; Plant Extracts ; pharmacology ; therapeutic use ; Soybeans ; chemistry

Baicalein, a flavonoid compound extracted from dried roots of traditional Chinese medicine Scutellaria baicalensis, has been widely applied as an antioxidant and anti-inflammatory agent. With continuous studies on its mechanisms, recent findings suggest that baicalein has some effect on neuroprotection and improvement of clinical symptoms in neurodegenerative diseases such as Parkinson's disease. Recent studies showed that its neuroprotective efficacy is closely related to such functions as antiinflammatory, antioxidative stress, protecting chondriosome, inhibiting glutamate neurotoxicity, promoting nerve growth and inhibiting alpha-synuclein protein-aggregate activities. The aim of this article is to summarize the neuroprotective effects of baicalein in Parkinson's disease.
Flavanones ; pharmacology ; therapeutic use ; Humans ; Mitochondria ; drug effects ; metabolism ; Nerve Growth Factor ; metabolism ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Oxidative Stress ; drug effects ; Parkinson Disease ; drug therapy ; metabolism ; pathology

Wogonin is a kind of natural flavonoid compound. According to findings in the latest studies, wogonin shows a wide range of antitumor effects, with the characteristics of multi-pathway, multi-link and multi-target, such as promoting tumor cell apoptosis through ROS or Ca(2+)-mediated signal paths, enhancing tumor cytotoxicity by TNF-α and TRAIL, blocking tumor cell cycle, inhibiting tumor angiogenesis and resisting cancer synergistically with chemotherapeutic drugs. Moreover, Wogonin could enhance body immune function by enhancing immune cell infiltration, regulating the immune cell phenotype and promoting relevant cytokine secretion. In this paper, the authors summarized the advance in studies on wogonin's antitumor and immunomodulatory effects.
Animals ; Antineoplastic Agents ; therapeutic use ; Apoptosis ; drug effects ; Drugs, Chinese Herbal ; therapeutic use ; Flavanones ; therapeutic use ; Humans ; Immunologic Factors ; therapeutic use ; Neoplasms ; drug therapy ; immunology ; physiopathology ; Tumor Necrosis Factor-alpha ; genetics ; immunology

Wogonin is a plant flavonoid compound extracted from Scutellaria baicalensis (Huang-Qin or Chinese skullcap) and has been studied thoroughly by many researchers till date for its anti-viral, anti-oxidant, anti-cancerous and neuro-protective properties. Numerous experiments conducted in vitro and in vivo have demonstrated wogonin's excellent tumor inhibitory properties. The anti-cancer mechanism of wogonin has been ascribed to modulation of various cell signaling pathways, including serine-threonine kinase Akt (also known as protein kinase B) and AMP-activated protein kinase (AMPK) pathways, p53-dependent/independent apoptosis, and inhibition of telomerase activity. Furthermore, wogonin also decreases DNA adduct formation with a carcinogenic compound 2-Aminofluorene and inhibits growth of drug resistant malignant cells and their migration and metastasis, without any side effects. Recently, newly synthesized wogonin derivatives have been developed with impressive anti-tumor activity. This review is the succinct appraisal of the pertinent articles on the mechanisms of anti-tumor properties of wogonin. We also summarize the potential of wogonin and its derivatives used alone or as an adjunct therapy for cancer treatment. Furthermore, pharmacokinetics and side effects of wogonin and its analogues have also been discussed.
Animals ; Antineoplastic Agents, Phytogenic ; pharmacology ; therapeutic use ; DNA Adducts ; metabolism ; Drug Resistance, Neoplasm ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Flavanones ; pharmacology ; therapeutic use ; Humans ; Neoplasms ; drug therapy ; metabolism ; Phytotherapy ; Scutellaria baicalensis ; chemistry ; Signal Transduction ; drug effects

OBJECTIVETo evaluate the influence of naringin on PMMA-induced osteoclastic bone resorption using the mouse air sacs model.

METHODSTotal 48 female Balb/c mices with the age of 8 to 10 weeks were chosen in the study. Air were injected into the back in 32 mices and formed the air sacs, 6 d later, the skulls (originated from other 16 mices) were implanted to the air sacs. Thirty-two animals were divided into naringin treatment group (with 2 concentrations of 150 mg/kg and 30 mg/ kg) , DMSO group and PBS blank group, 8 animals in each group. Polymethylmethacrylate (PMMA) particles were injected into the air sacs in naringin treatment groups and DMSO group so as to irritate inflammatory reaction. Naringin with 2 concentrations of 150 mg/kg and 30 mg/kg were dissolved in DMSO of 0.2 ml, and were injected into air sacs, respectively. In PBS black group, no stimulation with PMMA particles, only injected PBS, and in DMSO group, injected DMSO without naringin. Tartrate resistant acid phosphatase (TRAP), Ca2+ release, modified Masson stain and histological analysis were performed on the 7th day after stimulation.

RESULTSCompared with DMSO group, naringin treatment group's cellular infiltration decreased (P < 0.01); concentration of 150 mg/kg was better than that of concentrations of 30 mg/kg (8.90 ± 1.75 vs 15.23 ± 1.86). Naringin can decrease calcium release in the lavage of the air sacs bone resorption model, especially obvious in naringin with concentration of 150 mg/kg. Naringin can ameliorate the inflammatory reaction and the subsequent bone resorption (including bone collagen loss, TRAP positive cells amount and so on) in air sacs with bone implant and PMMA particles. Naringin with concentration of 150 mg/kg appeared to be an optimal dosage to deliver the therapeutic effects.

CONCLUSIONNaringin inhibits PMMA-induced osteoclastogenesis and ameliorates the PMMA-associated inflammatory reaction and the subsequent bone resorption.

Animals ; Disease Models, Animal ; Female ; Flavanones ; therapeutic use ; Mice ; Mice, Inbred BALB C ; Osteoclasts ; drug effects ; physiology ; Osteolysis ; chemically induced ; prevention & control ; Polymethyl Methacrylate ; toxicity

The present study was designed to isolate and characterize the analgesic compounds of Artemisa sacrorum Ledeb. The EtOAc crude extracts from the aerial parts of Artemisa sacrorum Ledeb were separated by chromatography and the structures of new compounds were elucidated based on spectral analyses. Analgesic activities of the isolated compounds were assessed in rats with hot plate test and paw pressure assay. Two new flavone C-glycosides, named as Sacroroside A and B (Compounds 1 and 2) were isolated from the EtOAc crude extract of the aerial parts ofArtemisa sacrorum Ledeb. They showed significant analgesic effects. In conclusion, Compounds 1 and 2 are new natural products, which show significant analgesic effects in a dose-dependent manner.
Analgesics ; chemistry ; isolation & purification ; pharmacology ; therapeutic use ; Animals ; Artemisia ; chemistry ; Disaccharides ; chemistry ; isolation & purification ; pharmacology ; therapeutic use ; Flavanones ; chemistry ; isolation & purification ; pharmacology ; therapeutic use ; Flavones ; chemistry ; isolation & purification ; pharmacology ; therapeutic use ; Hot Temperature ; Male ; Molecular Structure ; Pain ; drug therapy ; Phytotherapy ; Plant Components, Aerial ; Plant Extracts ; chemistry ; pharmacology ; therapeutic use ; Pressure ; Rats, Wistar

Adult ; Drug Therapy, Combination ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Flavanones ; Flavonoids ; therapeutic use ; Flowers ; chemistry ; Humans ; Intracranial Hemorrhage, Traumatic ; drug therapy ; Male ; Middle Aged ; Phytotherapy ; Plants, Medicinal ; chemistry

This paper was aimed to observe the interventional effect of Sedum sarmentosum total flavanones on hepatic fibrosis and its possible mechanism through the subcutaneous injection of CCl_4 in rats. Sixty male SD rats were randomly divided into normal control group, model group, low-dose, medium-dose, high-dose S. sarmentosum total flavanones groups(100, 200, 400 mg·kg~(-1)) and silymarin group(200 mg·kg~(-1)). The model of liver fibrosis was established by subcutaneous injection of rats with 40% CCl_4. After the modeling, the drug groups were intragastrically administered with corresponding drugs once a day for consecutively five weeks, while the normal group and the model group were given 0.9% sodium chloride solution during the same period. After the experiment, the general conditions of rats and the pathological changes of liver tissues were observed, and the contents of serum ALT, AST, HA and LN were measured. Besides, the expressions of the protein and relevant mRNA of Smad2/3, Smad4 and α-SMA in rats were detected. Compared with model group, S. sarmentosum total flavanones could significantly increase the rats' body weight, inhibit the increase of liver and spleen index in rats of liver fibrosis, reduce the levels of ALT, AST, HA and LN, and alleviate pathological changes. Meanwhile, compared with the model group, the protein expressions of Smad2/3, Smad4 and α-SMA as well as relevant mRNA expressions in S. sarmentosum total flavanones group were obviously decreased, while Smad7 expression was markedly increased. As a result, S. sarmentosum total flavanones could significantly alleviate CCl_4-induced liver fibrosis, and its anti-hepatic fibrosis mechanism may be related to intervention with Smads pathway, so as to inhibit the activation of HSC.
Animals ; Carbon Tetrachloride ; Drugs, Chinese Herbal/therapeutic use* ; Flavanones/therapeutic use* ; Hepatic Stellate Cells/drug effects* ; Liver ; Liver Cirrhosis/drug therapy* ; Male ; Rats ; Rats, Sprague-Dawley ; Sedum/chemistry* ; Signal Transduction ; Smad Proteins/metabolism*

AIMTo explore the effect of baicalein (Bai-Chinese Traditional Medicine) on bleomycin (BLM)-induced fibrosis in lungs of rats and its possible mechanism.

METHODSSixty-eight male Sprague-Dawley rats were randomly divided into 4 groups: BLM plus Bai group, BLM plus normal saline (NS) group, NS plus Bai group, and NS plus NS group. The rats were received single intratracheal instillation of BLM (5 mg kg(-1) bw) or equal volume of NS as control, and received intraperitoneal injection o f Bai (12.5 mg x kg(-1) bw) or the same volume of NS asvehicle for 28 d. The hydroxyproline content, the collagen area, the mRNA expression of Col I (alpha), and the myofibroblasts in lung were examined.

RESULTSThe content of hydroxyproline, the percentage of collagen area, the mRNA expression of Col I (alpha), and the amount of myofibroblast were increased in lungs of rats on day 28 after intratracheal instillation of BLM, compared with that in lungs of the control rats, respectively( All P < 0.01). The above abnormal changes were ameliorated by Bai (12.5 mg x kg(-1) x d(-1) ip, x 28 d (All P < 0.05).

CONCLUSIONBai has anti-action on BLM-induced fibrosis in lung, and that the above action of Bai is related to the blockage of synthesis of type I collagen and the decrease of myofibroblast in lung.

Animals ; Bleomycin ; Collagen Type I ; genetics ; metabolism ; Flavanones ; pharmacology ; therapeutic use ; Male ; Myofibroblasts ; cytology ; Pulmonary Fibrosis ; chemically induced ; drug therapy ; physiopathology ; RNA, Messenger ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo observe the protective effect of active fractions of Huanglian Jiedu Decoction (HJD) on primary cortical neuron injury after oxygen-glucose deprivation (OGD)/reperfusion (R) injury. Methods Using macroporous resin method, HJDFE30, HJDFE50, HJDFE75, and HJDFE95 with 30%, 50%, 75%, and 95% alcohol were respectively prepared. Then the content of active components in different HJD fractions was determined with reverse phase high-performance liquid chromatography (RP-HPLC). The OGD/R injury model was induced by sodium dithionite on primary cortical neurons in neonate rats. MTT assay was used to observe the effect of four fractions (HJDFE30, HJDFE50, HJDFE75, and HJDFE95) and seven index components of HJD on the neuron viability.

RESULTSRP-HPLC showed active component(s) contained in HJDFE30 was geniposide; baicalin, palmatine, berberine, and wogonside contained in HJDFE50; baicalin, berberine, baicalein, and wogonin contained in HJDFE75. The neuron viability was decreased after OGD for 20 min and reperfusion for 1 h, (P <0. 01), and significantly increased after administered with HJD, HJDFE30, HJDFE50, and HJDFE75 (P <0. 05, P <0. 01). Geniposide, baicalin, baicalein, palmatine, wogonside, and wogonin could increase the cortical neuron viability (P <0. 05, P <0. 01).

CONCLUSIONSHJDFE30, HJDFE50, and HJDFE75, as active fractions of HJD, had protective effect on primary cortical neuron injury after OGD/R. Furthermore, geniposide, baicalin, and baicalein were main active components of HJD.

Animals ; Berberine ; Berberine Alkaloids ; Chromatography, High Pressure Liquid ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Flavanones ; Flavonoids ; Glucose ; metabolism ; Iridoids ; Models, Animal ; Neurons ; Oxygen ; metabolism ; Rats ; Reperfusion Injury ; drug therapy