Neuroprotective effects of Epigallocatechin-3-gallate (EGCG) in optic nerve crush model in rats.

Epigallocatechin-3-gallate (EGCG), the major catechin found in green tea, is a powerful antioxidant and has anti-inflammatory with neuroprotective potential. This study aims to investigate the neuroprotective effects of EGCG in an optic nerve crush (ONC) model in rats. Seventy-two Wistar rats were randomly divided into four groups: normal control (group A), sham operation+EGCG (group B), ONC+vehicle (group C), and ONC+EGCG (group D). The rats were treated intraperitoneally and orally with either vehicle or EGCG (25 mg/kg, injected daily for 5 days and 2 mg/kg orally daily afterwards). Two days after the first injection, an ONC injury was performed by using a micro optic nerve clipper with 40 g power at approximately 2 mm from the optic nerve head for 60 s. Fluorogold was injected into the bilateral superior colliculi 5 days before sacrifice and fluorescent gold-labelled retinal ganglion cells (RGCs) were counted under fluorescence microscopy on days 7, 14 and 28 after ONC. The expression of Neurofilament triplet L (NF-L) was measured via immunohistochemical and Western blotting analysis. In group C, a progressive loss of RGCs was observed after ONC. In contrast, the density of RGCs was significantly higher in group D (p=0.009, independent samples t-test) on day 7 after ONC, and statistical differences were obtained on days 14 and 28 (p=0.026 and p=0.019, respectively, independent samples t-test). The results of immunohistochemical and Western blotting analysis showed significantly higher NF-L protein expression in group D in comparison with group C on days 7, 14 and 28 after ONC. These findings suggest that there are protective effects of EGCG on RGCs after ONC, indicating EGCG might be a potential therapeutic agent for optic nerve diseases.

A new steroidal saponin, yuccalan, from the leaves of Yucca smalliana.

An extract of the leaves of Yucca smalliana Fern. (Agavaceae) showed potential antimicrobial activity. Employing a bioassay linked fractionation method, one of the active principles, namely yuccalan, was isolated as a new steroidal saponin. The structure of the new steroidal saponin was elucidated as 3-O-beta-D-glucopyranosyl-(1-->6)-beta-D-glucopyranosyl-(3beta, 5alpha, 6alpha, 25S)-spirostan-3,6,27-triol (1) using various spectroscopic techniques, including IR, MS, 1D and 2D 1H-NMR, and 13C-NMR. The purified yuccalan showed antifungal activities against both Rhizoctonia solani and Fusarium oxysporum.

Increased iron deposition in rat liver fibrosis induced by a high-dose injection of dimethylnitrosamine.

Using a developed rat model of hepatic necrosis and subsequent fibrosis induced by a high-dose intraperitoneal injection of dimethylnitrosamine (DMN), we studied iron deposition and expression of transforming growth factor-beta(1) (TGF-beta(1)) during the development of persistent liver fibrosis. Rats were sacrificed at several timepoints from 6 h to 10 months post-injection and the livers were examined for iron content and distribution, and for expression of alpha-smooth muscle actin, ED-1, TGF-beta(1), and collagen (alpha(2))I. Morphologic evidence of acute submassive hemorrhagic necrosis peaked at 36 h; on day 3 the residual parenchyma contained activated hepatic stellate cells (HSCs) and necrotic areas contained numerous macrophages; and on day 5, necrotic tissues and erythrocytes had been phagocytosed and macrophages contained abundant iron deposits. From days 7 to 10, iron-laden macrophages and activated HSCs (myofibroblasts) populated the fibrous septa in parallel. From week 2 to month 10, closely arranged macrophages and myofibroblasts were found in central-to-central bridging fibrotic tissue. TGF-beta(1) was strongly detected in both macrophages and HSCs during development of liver fibrosis. Our data suggest that increased iron deposition may be involved in the initiation and perpetuation of rat liver fibrosis. Iron-laden macrophages may influence HSCs through the action of TGF-beta(1) in DMN-induced liver fibrosis.