Effects of Dietary Supplementation with Sea Buckthorn (Hippophae rhamnoides L.) Seed Oil on an Experimental Model of Hypertensive Retinopathy in Wistar Rats.

BACKGROUND/AIMS: Sea buckthorn (Hippophae rhamnoides L.) oil is a rich source of phytosterols, flavonoids, unsaturated fatty acids, and carotenoids, known for their antioxidant and neuroprotective activity. In this study, we investigated the neuroprotective and antioxidant effect of sea buckthorn oil on rat retina in hypertensive retinopathy. METHODS: Twenty-eight male 6-month-old Wistar rats were separated into 3 groups: (1) controls, (2) unilateral nephrectomized rats receiving drinking water with 1% NaCl, (3) unilateral nephrectomized rats receiving 0.5 mL sea buckthorn oil and drinking water with 1% NaCl. Systemic pressures were being measured with the tail-cuff method. The antiapoptotic effect of sea buckthorn was determined by measuring glial fibrillary acidic protein (GFAP), cleaved caspase-3, and glutamine synthetase levels with immunohistochemistry and Western blot. RESULTS: Nephrectomy and salt intake caused increases in both systolic and diastolic pressures. Both types of analysis showed that group 2 had statistically significant increases in the expression of GFAP and cleaved caspase-3, while group 3 showed no significant differences compared with the control group. The expression of glutamine synthetase showed no significant differences between the 3 groups. CONCLUSIONS: Our findings suggest that sea buckthorn could notably protect the retina from damage induced by hypertensive retinopathy.

EGFR and c-Jun exhibit the same pattern of expression and increase gradually during the progress of oral oncogenesis.

BACKGROUND: Epidermal growth factor receptor (EGFR) and c-Jun oncogenes are implicated in the same pathway of signal transduction affecting cell differentiation. In order to investigate their possible correlation with sequential histological stages of OSCC formation, we established an experimental model of induced oral carcinogenesis in Syrian golden hamsters. MATERIALS AND METHODS: Thirty-seven animals were divided into one control group (n=7) and three experimental groups (n = 10 each), which were treated with a carcinogen and sacrificed at 10, 14 and 19 weeks after treatment. Tumour sections were studied using monoclonal antibodies against EGFR and c-Jun proteins. RESULTS: The same pattern of expression was observed for both oncogenes, with a significant gradual increase of positively stained cells throughout oral carcinogenesis. CONCLUSION: Since EGFR and c-Jun are implicated in the same molecular pathway of signal transduction, it may be assumed that an increase in EGFR levels leads to increased activation of phospholipase Cy signal transduction cascade, which in turn activates c-Jun protein. Therefore, c-Jun expression in oral cancer seems to be increased through the EGFR-PLCy-Raf-MEK-ERK pathway and not the H-ras-Raf-MEK-ERK/JNK pathway.