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Summary Irinotecan is one of the most important anti‐tumour drugs against a broad spectrum of malignancies, but is known to be associated with possible oral complications. The aim of the present study was to evaluate the effect of irinotecan on the tongue mucosa of juvenile male albino rat at adulthood using different histological and immunohistochemical methods. Twenty juvenile male albino rats were divided equally into two groups: control and irinotecan‐treated group (single injection of 200 mg irinotecan/kg, then kept for four weeks without treatment). The tongue specimens were processed for light microscopy and scanning electron microscopy. The irinotecan‐treated group showed statistically significant shortening and thinning of the lingual papillae. There was loss of the normal appearance of the filiform papillae with focal cell loss alternating with areas of hyperkeratosis. Focal separation of the keratin layer, some nuclear changes and vacuolation of some epithelial cells were detected. Dilated congested blood vessels and mild mononuclear cellular infiltration were encountered. Atrophic fungiform papillae with ill‐defined taste bud cells were observed. A statistically significant decrease in the pattern of Ki67 immunohistochemical staining reaction was detected in comparision to the control group. Scanning electron microscopy revealed different signs of atrophy of the tongue papillae. Focal areas of desquamation of lingual papillae were observed revealing some filiform papillae with desquamated surface, bisected tips and evident thinning. Some extravasated red blood cells could be detected. Thus irinotecan caused significant morphological and morphometrical alterations of the tongue mucosa in particularly the filiform papillae.

Background: Capecitabine is a chemotherapeutic agent widely used for the treatment of malignancies. Ocular disorders have been reported with capecitabine therapy. Hesperidin is a naturally occurring compound derived mainly from citrus fruits and has a wide range of pharmacological activities and a proposed role in combating many ocular diseases. Aim: To evaluate the potential protective role of hesperidin against the corneal toxicity caused by capecitabine in adult male albino rats. Material and Methods: Thirty-six adult male albino rats were divided into four equal groups; control group, hesperidintreated group (50 mg/kg), capecitabine-treated group (40 mg/kg), and combination-treated "capecitabine and hesperidintreated" group. Animals were orally administered once daily for one month. Specimens from the cornea were processed for light and electron microscopy. Immunohistochemical study was performed using antibodies against p53. Results: Specimens from capecitabine-treated animals showed significant decrease of epithelial thickness. The corneal epithelial cells showed nuclear alteration and vacuolated cytoplasm. The stromal collagen fibers were irregularlyarranged and widely separated with neovascularization and mononuclear cellular infiltration. Ultrastructurally, focal widening of the intercellular spaces, partial loss of desmosomal junctions and swollen mitochondria were observed. The immunohistochemical study showed a significant increase in p53 immunoreaction. In contrast, minimal changes were observed in rats treated concomitantly with both capecitabine and hesperidin, with a non significant increase in the immunoreactions. Conclusion: Capecitabine induced structural changes in cornea of adult albino rat that could be ameliorated by concomitant treatment with hesperidin.

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The lung is one of the most sensitive organs that are vulnerable to injuries induced by lower limb ischemia-reperfusion. Scutellarin is a flavonoid glycoside extracted from the Chinese herb Erigeron breviscapus. This study aimed to investigate the role of scutellarin in ameliorating lung injury in a rat model of bilateral hind limb ischemia-reperfusion. Twenty-four adult male albino rats were equally divided into four groups; control, scutellarin, bilateral hind limb ischemia-reperfusion, and bilateral hind limb ischemia-reperfusion followed by scutellarin (at a dose of 20 mg/kg/day for 14 days). Lung specimens were processed for different biochemical and histological techniques. The bilateral hind limb ischemia-reperfusion group showed a significant increase in lung malondialdehyde and myeloperoxidase levels as well as a significant decrease in lung glutathione and superoxide dismutase. Histological examination revealed collapsed alveoli, polymorphic mononuclear cell infiltration, thickened dilated congested blood vessels, and excessive collagen fiber deposition in thickened interalveolar septa. A significant increase in iNOS and Bax immunohistochemical expression was associated with a significant decrease in Bcl2 and COX2 expression. Scutellarin administration following bilateral hind limb ischemia-reperfusion significantly ameliorated all studied parameters. It can be concluded that scutellarin could be beneficial in improving bilateral hind limb ischemia-reperfusion-induced lung damage most probably through its antioxidant, anti-inflammatory, and antiapoptotic effects.

Background: Tartrazine is one of the azo dyes that are the most common artificial food colors widely used in many food products. Tartrazine is used in many developing countries without strict regulations. Aim of the study: to investigate the effect of tartrazine on the gastric mucosa and to evaluate the possible role of recovery after its withdrawal with or without riboflavin in rat. Materials and Methods: Twenty-four adult male albino rats were equally divided into 4 groups; Control, riboflavin, tartrazinetreated group (orally administered 200 mg/kg/day tartrazine for 60 days), tartrazine-recovery group (orally administered 200 mg/kg/day tartrazine for 60 days then left without treatment for another 60 days) and tartrazine-recovery and riboflavin group (that were orally administered tartrazine for 60 days then stopped and followed with riboflavin for another 60 days). Glandular stomach specimens were processed for histological and immunohistochemical techniques. Results: Tartrazine-treated group depicted variable degrees of mucosal lesions with significant decrease in its thickness. Parietal cells with vacuolated cytoplasm and irregular nuclei, and vacuolated chief cells with pyknotic nuclei were detected. Dilated congested blood vessels and aggregated mononuclear cells were observed. Ultrastructural examination showed parietal and chief cells with condensed nuclei and dilated rough endoplasmic reticulum. Tartrazine-recovery group showed almost intact gastric mucosa. Tartrazine-recovery with riboflavin group showed a near normal gastric mucosa. Both Ki67 and iNOS-immunohistochemical expression showed a statistically significant increase upon tartrazine administration coupling to a significant decrease in Periodic-Acid-Schiff expression. Tartrazine-recovery group still revealed significant differences in these parameters compared to the control, while tartrazine-recovery with riboflavin showed non-significant differences from the control. Conclusion: Tartrazine affected the stomach and was alleviated by stopping it. Combined recovery along with riboflavin was more efficient on the recovery of gastric mucosa.

Parkinson’s disease (PD) is the second most common neurodegenerative disease, frequently associated with a gastric ulcer. We aimed to investigate the adropin neuroprotective/gastroprotective potential in the indomethacin (IND)-induced gastric ulcer in a rotenone-induced PD model. Rats were randomly divided into four groups: normal control group, rotenone/IND treated (PD /Ulcer) group, adropin treated PD/Ulcer group, and l-dopa/omeprazole (Om) treated PD/Ulcer group. There were ten rats selected for the normal control group. Striatal dopamine (DA), apoptosis/redox status, and motor/behavioral impairments were evaluated. Gastric oxidative stress, H+/K+-ATPase activity, prostaglandin E2, mucin content, and von Willebrand factor were measured. Gastric/striatal phosphatidylinositol 3-kinase (PI3K)/phosphorylated Akt and gastric vascular endothelial growth factor (VEGF)/striatal P53 immunoreactivities were checked. Striatal P53 upregulated modulator of apoptosis (Puma)/gastric vascular endothelial growth factor receptor-2 (Vegfr-2) expressions were evaluated. Adropin successfully restored striatal DA and attenuated rotenone-induced motor/behavior deficits along with strong gastroprotective potential, possibly through antioxidant activity via reduction in malondialdehyde level and upregulated superoxide dismutase, catalase activities, and serum ferric reducing antioxidant power. Adropin restored the delicate balance between the defective pro-survival PI3K/Akt/murine double minute 2 signals and apoptotic P53/Puma pathways. Adropin can be considered as a uniquely attractive therapeutic target in PD and its associated gastric ulcer.

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