Long-term Treatment with Oriental Medicinal Herb Artemisia princeps Alters Neuroplasticity in a Rat Model of Ovarian Hormone Deficiency.

Artemisia princeps (AP) is a flowering perennial used as a traditional medicine and dietary supplement across East Asia. No study has yet assessed its effects on synaptic plasticity in hippocampus and much less in a model of ovarian hormone deficiency. We examined the influence of chronic oral AP ethanol extract treatment in ovariectomized rats on the induction of long-term depression in a representative synapse (CA3-CA1) of the hippocampus. Ovariectomized rats demonstrated lower trabecular mean bone mineral densities than sham, validating the establishment of pathology. Against this background of pathology, AP-treated ovariectomized rats exhibited attenuated long-term depression (LTD) in CA1 relative to water-treated controls as measured by increased field excitatory post-synaptic potentials (fEPSP) activation averages over the post-stimulation period. While pathological significance of long-term depression (LTD) in ovariectomized rats is conflicting, that AP treatment significantly affected its induction offers justification for further study of its influences on plasticity and its related disorders.

The anti-obesity effect of Lethariella cladonioides in 3T3-L1 cells and obese mice.

The aim of this study was to investigate whether a water extract of L. cladonioides (LC) has an anti-obesity effect in 3T3-L1 cells and obese mice. Treatment of differentiated 3T3-L1 adipocytes with LC caused a significant increase in glycerol release and reduced the protein expression of the adipogenic transcription factors, PPARγ and C/EBPα. In an animal model, obese mice were artificially induced by a high fat diet for 10 weeks. Experimental groups were treated with LC (100 mg/kg/day) by gavage for the next 10 weeks. At the end of experiment, the body weight of the LC group mice was reduced by 14.2% compared to the high fat diet (HFD) group. The treatment also decreased liver (31.0%), epididymal (18.0%) and retroperitoneal (19.3%) adipose tissue, and kidney (6.7%) weights, respectively, compared with those of the HFD group. LC prevented diet-induced increases in the serum level of TC (22.6%), TG (11.6%), and glucose (35.0%), respectively, compared with the HFD group. However, the HDL-C level was higher in the LC group (26.1%) than the HFD group. The results of this study thus suggest that LC suppressed lipid accumulation and expression of adipogenic transcription factors, and increased the amount of glycerol release. LC also indicated an anti-obese and anti-hyperlipidemic effect.

Chlorella methanol extract reduces lipid accumulation in and increases the number of apoptotic 3T3-L1 cells.

Obesity is a fast-growing problem that is reaching pandemic proportions. Chlorella has many biological merits for promoting health, including detoxification, boosting the immune system, and even reversing cancer. In this study, we found that methanol extract of Chlorella reduces lipid accumulation in 3T3-L1 adipocytes. It has been postulated that these antiobesity effects could be a result of reducing adipogenesis. First, the MTT assay indicated that Chlorella significantly inhibited cell growth of 3T3-L1 preadipocytes. The accumulation of triacylglycerol in 3T3-L1 adipocytes decreased in cells treated with Chlorella versus those in untreated cells by Oil Red O staining. In parallel, Chlorella showed a significant dose-dependent increase in lactate dehydrogenase activity in culture medium of differentiated 3T3-L1 adipocytes. Second, we investigated the effects of Chlorella on the induction of apoptosis by fluorescence-activated cell sorting analysis. Chlorella showed that apoptotic cells increased in a time- and dose-dependent manner in cell apoptosis analysis by propidium iodide (PI) staining. Treatment with Chlorella decreased the number of normal cells and increased the number of apoptotic cells in a dose-dependent manner in annexin V-fluorescein isothiocyanate/PI double staining. Therefore, Chlorella is expected to efficiently reduce adipogenesis in 3T3-L1 adipocytes and to induce apoptosis in 3T3-L1 preadipocytes.

Growth-inhibitory and proapoptotic effects of alpha-linolenic acid on estrogen-positive breast cancer cells.

We tested the anticarcinogenic effect of alpha-linolenic acid (ALA) as a single compound. To test the role of ALA in breast cancer cells (MCF-7), we analyzed the antiproliferative pathway and the proapoptotic pathway. ALA exhibited growth inhibition on MCF-7 cells dose-dependently of ALA in 24, 48, and 72 h, without possible cytotoxicity per se. ALA enhanced the cell growth-inhibitory activity in a dose-dependent manner. Second, the proapoptotic pathway showed a sub-G(1) accumulation with concomitant upregulation of proapoptotic Bax expression, as well as a downregulation of antiapoptotic Bcl-2 expression dose-dependently, causing the Bcl-2/Bax ratio to decrease by about 50%. Subsequent cytochrome c release and proteolytic activation of caspase-3 followed by proteolytic cleavage of poly(ADP-ribose) polymerase all suggest ensuing progression to apoptosis. This finding suggests that ALA alone might also be responsible for growth-inhibitory and proapoptotic effects on estrogen-positive breast cancer cells.