[Gallnut and its identification as a herb in traditional Chinese medicine].

Gallnut (Mo Shi Zi), as one of the herbs popularly used in traditional Chinese medicine, came into China from Persia in the Northern Wei Dynasty. Gallnut was translated into different names from Persian into Chinese. This study attempted to identify its names, sources and nature by starting with Mo Shi Zi () and comparing with its relevant names Mo Shi Zi(),Ba Lv Zi () and Wu Bei Zi (). It was found that'', meaning black, in Mo Shi Zi () did not make sense because it neither matched the pronunciation in translation nor interpreted the medical meaning of Mo Shi Zi (). Mo Shi Zi () and Ba Lv Zi() were the same herb in traditional Chinese medicine. In Greek and Arabic classic books, Bullut referred to oak groups and their galls, but not Ba Lv Zi (). Ba Lv Zi () in these books referred to Omphacitis. Mo Shi Zi () referred to insect galls in the family of Quercus infectoriain Xi Yao Da Cheng, a book from overseas, and Wu Bei Zi ()appeared in the annotated text of Mo Shi Zi () as a similar herb. It was found that in traditional Chinese medicine, Mo Shi Zi () and Wu Bei Zi( ) were two different herbs, but could be interchanged in their medical nature.

Cantharidin suppressed breast cancer MDA-MB-231 cell growth and migration by inhibiting MAPK signaling pathway.

As an active constituent of the beetle Mylabris used in traditional Chinese medicine, cantharidin is a potent and selective inhibitor of protein phosphatase 2A (PP2A) that plays a crucial role in cell cycle progression, apoptosis, and cell fate. The role and possible mechanisms exerted by cantharidin in cell growth and metastasis of breast cancer were investigated in this study. Cantharidin was found to inhibit cell viability and clonogenic potential in a time- and dose-dependent manner. Cell cycle analysis revealed that cell percentage in G2/M phase decreased, whereas cells in S and G1 phases progressively accumulated with the increasing doses of cantharidin treatment. In a xenograft model of breast cancer, cantharidin inhibited tumor growth in a dose-dependent manner. Moreover, high doses of cantharidin treatment inhibited cell migration in wound and healing assay and downregulated protein levels of major matrix metalloproteinases (MMP)-2 and MMP-9. MDA-MB-231 cell migration and invasion were dose-dependently inhibited by cantharidin treatment. Interestingly, the members of the mitogen-activated protein kinase (MAPK) signaling family were less phosphorylated as the cantharidin dose increased. Cantharidin was hypothesized to exert its anticancer effect through the MAPK signaling pathway. The data of this study also highlighted the possibility of using PP2A as a therapeutic target for breast cancer treatment.

Cantharidin suppressed breast cancer MDA-MB-231 cell growth and migration by inhibiting MAPK signaling pathway

As an active constituent of the beetle Mylabris used in traditional Chinese medicine, cantharidin is a potent and selective inhibitor of protein phosphatase 2A (PP2A) that plays a crucial role in cell cycle progression, apoptosis, and cell fate. The role and possible mechanisms exerted by cantharidin in cell growth and metastasis of breast cancer were investigated in this study. Cantharidin was found to inhibit cell viability and clonogenic potential in a time- and dose-dependent manner. Cell cycle analysis revealed that cell percentage in G2/M phase decreased, whereas cells in S and G1 phases progressively accumulated with the increasing doses of cantharidin treatment. In a xenograft model of breast cancer, cantharidin inhibited tumor growth in a dose-dependent manner. Moreover, high doses of cantharidin treatment inhibited cell migration in wound and healing assay and downregulated protein levels of major matrix metalloproteinases (MMP)-2 and MMP-9. MDA-MB-231 cell migration and invasion were dose-dependently inhibited by cantharidin treatment. Interestingly, the members of the mitogen-activated protein kinase (MAPK) signaling family were less phosphorylated as the cantharidin dose increased. Cantharidin was hypothesized to exert its anticancer effect through the MAPK signaling pathway. The data of this study also highlighted the possibility of using PP2A as a therapeutic target for breast cancer treatment.

Antiosteoporotic activity of icariin in ovariectomized rats.

Icariin was evaluated for its antiosteoporotic activity in an ovariectomized rat model of osteoporosis. The rats were divided into sham and OVX groups. The OVX rats were then subdivided into five groups treated with water, nylestriol (1 mg/kg body weight, weekly, orally) or icariin (ICA) (5, 25, and 125 mg/kg body weight, daily, orally) for 12 weeks. In OVX rats, the increases of body weight, serum BGP and ALP were significantly decreased by ICA treatment. In OVX rats, atrophy of uterus and descent of BMD were suppressed by treatment with ICA. In addition, ICA (125 mg/kg body weight) completely corrected the decreased serum concentration of Calcium, Phosphorus, and E(2) observed in OVX rats. ICA (125 mg/kg body weight) increased biomechanical strength significantly in comparison to the sham group. Histological results also showed its protective action through promotion of bone formation. The findings, assessed on the basis of biochemical, bone mineral density, biomechanical, and histopathological parameters, showed that ICA has a definite antiosteoporotic effect, similar to estrogen, especially effective for prevention bone fracture induced by estrogen deficiency.

Suppression of autoimmune disease by dietary n-3 fatty acids.

Previous studies have demonstrated that dietary fish oil preparations have anti-inflammatory effects in humans and in experimental animals, but the individual components of fish oils that are responsible for their anti-inflammatory effects have not been documented. We therefore investigated in (NZB x NZW)F1 mice, a model for human systemic lupus erythematosus, the effects of diets containing ethyl esters of two purified n-3 fatty acids, eicosapentaenoic acid (EPA-E) and docosahexaenoic acid (DHA-E), a refined fish oil triglyceride (FO) which contained 55% n-3 fatty acids, and beef tallow (BT) which contains no n-3 fatty acids. The diets were initiated prior to the development of overt renal disease at age 22 weeks, and continued for 14 weeks. The extent of the renal disease was quantified by light microscopy and by proteinuria. Diets containing either 10 wt% FO, 10% EPA-E, or 6% or 10% DHA-E alleviated the severity of the renal disease, compared to the BT diet, whereas diets containing either 3% or 6% EPA-E or 3% DHA-E were less effective. Two diets containing approximately 3:1 mixtures of EPA-E and DHA-E alleviated the renal disease to a greater extent than expected for either of these fatty acids given singly. We believe that these experiments provide the first demonstration of anti-inflammatory effects of individual dietary n-3 fatty acids. The results also indicate that the anti-inflammatory effects of fish oils depend on synergistic effects of at least two n-3 fatty acids.

Effect of fish-fat or beef-fat supplemented diet on immune complex-induced enteropathy in the rat.

In contrast to animals on a beef fat-supplemented diet (BFD), animals maintained on a fish fat-supplemented diet (FFD) incorporate increased amounts of eicosapentaenoic acid (EPA) into membrane phospholipids. Generation of lipid mediators from such tissues favors the formation of compounds with less pro-inflammatory activity than are derived from tissues poor in EPA. Nevertheless, the FFD has not had a uniformly beneficial effect on animal models of inflammatory diseases. We previously showed that intravenous injection of rat anti-BSA-BSA complexes (IC) prepared in 5x antigen excess rapidly induced a striate pattern of serosal (to mucosal) hemorrhage and vascular congestion throughout the small intestine. In this study, we tested the effect of a BFD and FFD on immune complex-induced enteropathy. After six (Expt. 1) or eight weeks (Expt. 2) on the diet, rats were injected with IC and the severity of serosal hyperemia in the small intestine was scored. In some FFD, no lesions were seen under conditions which elicited moderate to severe lesions in BFD rats. In Expt. 1 involving 22 rats and in Expt. 2 involving 28 rats, those on the FFD had a significantly lower composite lesional score compared to those on the BFD, p less than 0.005 and p less than 0.005, respectively. These results indicate that the FFD had a beneficial effect on IC-induced enteropathy. It is suggested that this effect of the FFD may be mediated primarily by a reduction in availability of platelet-activating factor.