الفهرس 
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Abstract
Gastric ulcer is a common health problem that affects the quality of life due to its dreadful implications. The most common causes of gastric ulcer include H. pylori infection, the prolonged usage of NSAIDs, stress, inappropriate diets, alcohol and smoking. The current therapeutic strategies for gastric ulcers face a major drawback due to increased antibiotic resistance which has led to a decreased H. pylori eradication rate alongside with NSAID-related side effects which mandate intensive searching for new antiulcerogenic modalities.
This study was designed to investgate the potential protective effect of sweet potato juice, carrot juice and their combination against the indomethacin-induced gastric ulcer in rats. Also total phenolics, antioxidant activity and carotenoids content of sweet potato juice and carrot juice were analyzed. The biochemical investigations include antioxidant, oxidant status, inflammatory and apoptotic effect as well as histopathological and immunohistochemical investigation.
In this study, sixty adult male albino rats, Sprague-Dawley strain, weighing 150g ± 5 fed on commercial pellet diet were divided into 6 groups, 10 rats for each as follows:
group (1): Rats were received (3 mL/kg b.wt.) distlled Water orally/day and served as healthy control group.
group (2): rats were received single dose of indomethacin (20mg/ kg b.wt.) suspended in 1% tween 80 orally to induce GU within 6 hrs. before scarification and served as positive controls.
group (3): SPJ+ GU, rats were received (3 mL/kg b.wt.) carrot juice orally/ day for 45 days, then received indomethacin to induce GU within 6 hrs. before scarification.
group 5: MJ + GU, rats were received (3 mL/kg b.wt.) mixed juice of sweet potato and carrot orally/ day for 45 days, then received indomethacin to induce GU within 6 hrs. before scarification.
group 6: Omp + GU, rats were received (20 mg/kg b.wt.) omeprazole drug orally/ day for 45 days, then received indomethacin to induce GU within 6 hrs. before scarification.
At the end of the experimental period, the following parameters were determined:
• Final body weight, body weight gain, food intake, FER and relative stomach weight
• Serum PGE2, COX-1, IL-6, TNF-α, CRP, Caspase-3, Pepsin, Hydroxyproline, NO, MDA, SOD, GSH and TAC levels.
• pH in gastric juice.
• HSP-70 gene expression in stomach tissues.
• Morphometric examination of stomach tissues.
• Percentage of ulcer surface area and ulcer inhibition.
• Histopathological examination of stomach sections for all experimental groups to confirm the biochemical results.
• Immunohistochemical study of Bax and Bcl-2 in stomach tissues.
The results of the present study could be summarized as follows:
1. Data revealed that each 1mL of tested sweet potato juice contains 85.5 mg as gallic acid equivalent of total phenols, 68.39 μg as trolox equivalent of total antioxidant capacity and each 100 mL contains 3.94 mg of total carotenoids. On the other hand, each 1mL of tested carrot juice contains 83.2 μg as gallic acid equivalent of total phenols, 53.58 μg as trolox equivalent of total antioxidant capacity and each 100 mL contains 13.56 mg of total carotenoids.
2. The biological results indicated that, groups which pre-treated with SPJ, CJ and MJ showed a significant decline in food intake by (-21.02 %), (-23.48%) and (-22.34%) respectively compared to gastric ulcer induced group, and as a consequence of decreased food intake, there was a significant reduction in body weight gain, feed efficiency ratio and relative stomach weight in the three pre-treated groups with the juices. In contrast there was no significant difference (p≤0.05) in food intake, body weight gain, feed efficiency ratio and relative stomach weight in gastric ulcer induced group and omeprazole pre-treated group compared to healthy control group.
3. The statistical analysis showed a significant decline in pH and hydroxyproline levels coupled with a significant elevation in pepsin level (p≤0.05) in gastric ulcer induced group compared with healthy control group. Pre-treatment with either SPJ, CJ and MJ induced significant ameliorative effect in the previously mentioned markers.
4. The results indicated a significant decrease in PGE2 and COX-1 with a significant elevation in the circulating CRP, TNF-α, IL-6 and caspase-3 levels in gastric ulcer induced group comparing to healthy control group (p≤0.05). Pre-treatment with SPJ, CJ and MJ showed a significant regression in the mean levels of both CRP, TNF-α and IL-6 with a significant elevation in PGE2 and COX-1 compared to gastric ulcer induced group. Furthermore, pre-treatment with the juices demonstrated a significant DROP in caspase-3 concentration on comparison with ulcerated rats by (-59.59%), (-47.91%) and (-59.18%) respectively.
5. It is clear from the results that there was statistically significant decline in antioxidant biomarkers (SOD, GSH and TAC) (p≤0.05) along with a significant increase in NO and MDA of gastric ulcer induced group when compared to healthy control group (p≤0.05). However, rats consumed SPJ and MJ showed a significant improvement in all these markers.
6. Regarding the gene expression results it was observed that the mRNA expression of HSP-70 was significantly downregulated in gastric ulcer induced group comparing to healthy control group. Also it was observed that the mRNA expression of HSP-70 in pre-treated groups with SPJ, CJ and MJ were upregulated significantly by comparing with gastric ulcer induced group.
7. The morphometric observations of stomach tissue showed that healthy control group had no ulcerations or lesions as well as normal color of the gastric mucosa. In contrast, gastric ulcer induced group exhibited a severe injury of the gastric mucosa that appears as deep and widespread of haemorrhagic lesions of different sizes. Moreover, the pre-treatment with SPJ or CJ exhibited mild and moderate superficial lesions in the gastric mucosa respectively. Additionally, the gastric lesions were reduced significantly in rats pre-treated with a MJ as well as omperazole respectively.
8. The results of the ulcer surface area and the percentage of ulcer inhibition indicated that, the total ulcerated surface area in gastric ulcer induced group was (9.20 ± 0.76). The pre-treatment with SPJ or CJ enhanced a reduction in ulcer surface area (1.64 ± 0.44) and (2.00 ± 0.63) respectively in comparison with gastric ulcer induced group. While the percentage of inhibition in SPJ and CJ is (82.17 %) and (78.27%) respectively. Meanwhile, the MJ shows a significant decrease in ulcerated surface area (0.86 ± 0.26) compared with the ulcer group with the increase in the inhibition percentage up to 90.65 %.
9. The histopathological investigations showed normal histoarchitecture of the gastric wall in healthy control group. While gastric ulcer induced group exhibited severe edema with abundant inflammatory cell infiltrate and congested blood vessels. In contrast treatment with SPJ and CJ showed a reduction in edema, inflammatory cell infiltrate as well as congested blood vessels. While MJ showed normal gastric wall with minimal edema, inflammatory cell infiltrate and congested blood.
10. The immunohistochemical sections of the healthy control group showed less detected immunoreaction in the gastric tissue for Bax and Bcl-2. In the gastric ulcer induced group, the quantitative analysis of Bax-immunoreaction revealed a significant increase (P≤0.05) with 20.95± 0.71 as a brown colour with a significant reduction (P≤0.05) up to 1.65±0.35 in immuno-expression of Bcl-2 in the gastric ulcer induced group compared with healthy control group. The pre-treatment with SPJ, CJ, MJ and Omp. significantly (P≤0.05) decreased Bax immunoreaction with the value of 11.85±0.72, 9.42±0.52, 5.62±0.31 and 7.00 ±0.39 respectively and increasing Bcl-2 immunoreaction levels up to 5.85± 0.35, 6.32±0.43, 7.08 ± 0.43 and 5.55 ± 0.22 respectively compared to the gastric ulcer induced group.
In conclusion, results showed that oral administration of SPJ, CJ and MJ could protect against the occurance of gastric ulcer induced by indomethacin in rats through antioxidant, anti-inflammatory and antiapoptotic effect.