ion.

To investigate the effect of Anastatica hierochuntica ethanolic (KEE), aqueous (KAE) extracts, and their combination against CCl4-induced hepatotoxicity in rats.

The HPLC analysis for KEE and KAE was quantitatively carried out. Biochemical liver markers, antioxidant enzymes, and histopathologicalalterations were examined then total hepatoprotection potential was calculated.

Among 9 identified phenolic compounds (PC) in KEA, sinapic acid was the highest while syringic acid was the highest among 21 identified PC in KAE. Six flavonoids were identified in KEE and two in KAE using HPLC, respectively. Oral administration of KEE, KAE, and KEE + KAE at 250 mg/kg body weight significantly reduced aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels, alkaline phosphatase (ALP), total bilirubin (TBILI), and also attenuated histopathological changes. Additionally, they reduced malondialdehyde (MOD), restored reduced-glutathione (GSH), and enhanced superoxide dismutase (SOD) levels. KEE, KAE, and KEE+KAE protected the liver from CCl4-hepatotoxicity as they mainly attenuating oxidative stress. Total hepatoprotection was about 128.3%, 114.5%, and 103.8% for KEE, KAE, and KEE+KAE, respectively.

Biochemical observations, supplemented by histopathological examination revealed thatAH affords extract-depending protection against CCl4-hepatotoxicity.

Biochemical observations, supplemented by histopathological examination revealed that AH affords extract-depending protection against CCl4-hepatotoxicity.

To further elucidate the mechanism underlying the anti-atherosclerotic effect of Dingxin recipe (DXR).

Fifty 6-week-old male ApoE-/- mice were randomly divided into the following groups model, simvastatin (5 mg·kg－1·d－1), DXR low-dose (9.30 g·kg－1·d－1), DXR middle-dose (18.59 g·kg－1·d－1) and DXR high-dose (37.18 g·kg－1·d－1) (n = 10). Ten male C57BL/6J mice were used as the control group. All ApoE-/- mice were fed a high-fat diet (HFD) and the control mice received a common diet. After HFD for 12 weeks, the mice were treated with DXR or simvastatin for another 12 weeks. The expression of inflammatory cytokines and visfatin was determined in serum and atherosclerotic lesions by enzyme-linked immunosorbent assay. Visfatin expression was also assessed in aortic atherosclerotic plaques. Cultured vessel endothelial cells (VECs) were pretreated with DXR sera prior to visfatin. The effects of DXR were analyzed to elucidate its protective mechanism against visfatin-induced inflammation in VECs.

DXR regulated blood lipids and reduced tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), intercellular adhesion molecules-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and visfatin expression in ApoE-/- mice, particularly at the higher doses. The areas of atherosclerotic lesions in the DXR groups were significantly smaller than those in the model group. DXR alleviated visfatin-induced VEC injury via downregulation of TNF-α, IL-6, ICAM-1 and VCAM-1 through mitogen-activated protein kinase pathways.

DXR alleviated atherosclerosis injury via downregulation of visfatin expression and inhibition of the visfatin-induced inflammatory response in VECs.

DXR alleviated atherosclerosis injury via downregulation of visfatin expression and inhibition of the visfatin-induced inflammatory response in VECs.

To investigate the efficacy of Lichong decoction (LD) from Traditional Chinese Medicine, on micro-angiogenesis in a mouse model of hysteromyoma.

A mouse model of hysteromyoma was developed by orthotopic intrauterine injection of primary human myoma cells isolated from patients from the Beijing Obstetrics and Gynecology Hospital into CB-17 Scid mice. Mice were administered high-dose LD, low-dose LD, mifepristone or water (control) daily by gavage for 4 weeks. Uterine diameter and coefficient (uterine weight/body weight) were measured. Uterine morphology was assessed by light microscopy (hematoxylin and eosin) and transmission electron microscopy. Serum levels of estradiol, progesterone, follicle-stimulating hormone and luteinizing hormone (LH) were measured by enzyme-linked immunosorbent assay. Uterine protein expression of hypoxia inducible factor (HIF)-1α, CD31 and proliferating cell nuclear antigen (PCNA) was detected by immunohistochemistry. VEGF and HIF-1α mRNAs were quantified by RT-PCR.

High-dose LD, low-dose LD and mifepristone reduced uterine diameter and coefficient, and attenuated the morphologic abnormalities associated with hysteromyoma. High-dose LD, low-dose LD and mifepristone inhibited hysteromyoma-induced micro-angiogenesis, as evidenced by a decrease in the number of new microvessels co-immunostaining for CD31 and PCNA (P < 0.01). check details High-dose LD and mifepristone lowered serum levels of estradiol, progesterone and LH (P < 0.05). High-dose LD, low-dose LD and mifepristone down-regulated HIF-1α mRNA and protein expressions and VEGF mRNA expression (P < 0.01).

The inhibition of hysteromyoma by LD may involve reductions in HIF-1α and VEGF expression and suppression of micro-angiogenesis.

The inhibition of hysteromyoma by LD may involve reductions in HIF-1α and VEGF expression and suppression of micro-angiogenesis.

To assess the effect of Jianpi Huazhuo Tiaozhi granules (JHTG) on oxidative stress damage to macrophages and explore the relationship between the levels of this damage and the nicotinamide adenine dinucleotide phosphate oxidase (NOX)/reactive oxygen species (ROS)- nuclear transcription factor kappa B (NF-κB) signaling pathway.

Macrophages cultured in vitro were divided into seven groups control, model control, inhibitor, positive control, 2.5% JHTG, 5% JHTG, and 10% JHTG. An oxidative stress injury model was established by stimulating macrophages with oxidized low-density lipoprotein. Cell survival and apoptosis were detected by 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide and flow cytometry assays, respectively. Malondialdehyde and superoxide dismutase levels were detected by enzyme-linked immunosorbent assays, while ROS levels were detected using a fluorescence probe. Proteins and mRNAs associated with the NOX/ROS-NF-κB pathway, including NOX4, p22phox, inhibitor of NF-κB kinase-α (IKK-α), inhibitor of NF-κB kinase-β (IKK-β), and NF-κB were detected by Western blot and PCR, respectively.