These results suggest that in patients with vascular complications of diabetes mellitus and even more in specific targeted organs, such as the eyes. Further study with larger sample size is recommended. In conclusion, the preoperative VEGF levels in both vitreous fluid and plasma were correlated with the Clofentezine progression of PDR after vitrectomy. The increased VEGF level in vitreous fluid may be identified as a significant predictive factor for the outcome of vitrectomy in patients with PDR. Further study of prospective design and comparison of the VEGF levels before and after surgery is recommended to confirm this conclusion. Sinigrin is a glucosinolate present in the seeds of Brassica nigra and other Brassicaceae family including broccoli and Brussels sprouts. Glucosinolates have been reported to exhibit different pharmacological properties in vitro. Sinigrin has been reported to exhibit anti-tumor activity. The metabolic activation of sinigrin leads to the formation of isothiocyanates which are believed to contribute to the anti-tumor activity. The therapeutic benefits of brassica vegetables and the anti-cancer activity of sinigrin in cancer cell lines are well established. The studies suggested that sinigrin could inhibit the cancer cell growth. An in vivo study reported the effects of the glucosinolates on carbohydrate and lipid metabolism in the rat model. Glucosinolates increased total cholesterol level, whereas the triacylglycerol levels in blood were found to be lowered. The glucosinolates are believed to lower the health risk of particular degenerative diseases. Glucosinolates are hydrolyzed to yield isothiocyanates which are excreted in the urine as an N-acetylcysteine conjugates. Sinigrin may also cause an increase in the activity of quinone reductase and glutathione-S-transferase in rats. However, the precise details of the pharmacological activity of sinigrin in rats are not currently available. In this study, different dosages of sinigrin were administered to the rats following liver damage. An in vitro study on liver cancer cells revealed that sinigrin could induce apoptosis. Cell 
cycle analysis showed that sinigrin induced cell cycle arrest at G0/G1 phase. In vivo studies revealed that sinigrin triggers over-expression of p53 and down-regulation of Bcl-2 family members and caspases. The results suggest that sinigrin exhibited anti-tumor activity in the liver and are consistent with a previous study of the impact of sinigrin on cancer cell lines. The inhibitory activity of sinigrin on carcinogen-induced liver damage was significantly attenuated. The gene expression of sinigrintreated HepG2 cells revealed that sinigrin induced apoptosis via a p53-dependent pathway. This result is reminiscent of analogous in vitro studies of isothiocyanates. In in vivo studies, rats after treatment with sinigrin showed an obvious change of body weight in different control and treatment groups. The body weight of the positive control group was significantly reduced. The results suggest the liver Oxysophocarpine function of the positive control group was attenuated compared with the treatment group. Effects of sinigrin treatment on the liver weight of different groups of rats are shown in Figure 3. The results showed that the liver weight of the positive control group was significantly increased whereas that of the treated group was reduced after treatment with sinigrin. These studies reflect the health benefits of sinigrin towards carcinogens-induced liver injury. The change in liver weight index in different treatment groups and the control groups are shown in Figure 4. These results indicate that the liver weight index of treatment groups of rats was reduced compared with that of the negative control group and the positive control group.