RESUMO
Background: Aquaporins (AQPs) are transmembrane channel proteins. Aquaporin 1 (AQP1), Aquaporin 3 (AQP3), and Aquaporin 7 (AQP7) are expressed in the jejunum. The purpose of this study was to ascertain how a high-fat high-fructose diet (HFFD) and intermittent fasting (IF) affect AQP1, AQP3, and AQP7 expression in the rat jejunum. Methods: Sixteen adult male rats were divided into control rats (n = 4) fed on a basal diet and water ad libitum for 12 weeks; IF control rats (n = 4) followed the IF protocol, HFFD-fed rats (n = 8) fed HFFD for eight weeks, and rats were randomized into two groups: HFFD only or HFFD and IF protocol from the beginning of the 9th week until the end of the experiment. The lipid profile values were assessed after 12 weeks. Jejunal oxidative markers (malondialdehyde and reduced glutathione) and AQP1, AQP3, and AQP7 mRNA expression were measured. Jejunal sections were used for morphometric analysis of villus length and crypt depth. Immunohistochemical evaluation of AQP1, AQP3, and AQP7 expression was also performed. Results: IF ameliorates HFFD-induced lipid profile, oxidative stress, and jejunal morphometric changes. The results of both mRNA expression using PCR and immunohistochemistry showed a significant increase in AQP1, AQP3, and AQP7 expression in HFFD, whereas IF caused a decline in this expression. Conclusion: These findings suggest that IF can reduce inflammation, and oxidative stress and restore jejunal morphology caused by HFFD.
RESUMO
Background: The majority of the suggested experimental modalities for peripheral nerve injury (PNI) result in varying degrees of recovery in animal models; however, there are not many reliable clinical pharmacological treatment models available. To alleviate PNI complications, research on approaches to accelerate peripheral nerve regeneration is encouraged. Cerebrolysin, dexamethasone, and ascorbic acid (vitamin C) drug models were selected in our study because of their reported curative effects of different mechanisms of action. Methodology: A total of 40 adult male albino rats were used in this study. Sciatic nerve crush injury was induced in 32 rats, which were divided equally into four groups (model, Cerebrolysin, dexamethasone, and vitamin C groups) and compared to the sham group (n = 8). The sciatic nerve sensory and motor function regeneration after crushing together with gastrocnemius muscle histopathological changes were evaluated by the sciatic function index, the hot plate test, gastrocnemius muscle mass ratio, and immune expression of S100 and apoptosis cascade (BAX, BCL2, and BAX/BCL2 ratio). Results: Significant improvement of the behavioral status and histopathological assessment scores occurred after the use of Cerebrolysin (as a neurotrophic factor), dexamethasone (as an anti-inflammatory), and vitamin C (as an antioxidant). Despite these seemingly concomitant, robust behavioral and pathological changes, vitamin C appeared to have the best results among the three main outcome measures. There was a positive correlation between motor and sensory improvement and also between behavioral and histopathological changes, boosting the effectiveness, and implication of the sciatic function index as a mirror for changes occurring on the tissue level. Conclusion: Vitamin C is a promising therapeutic in the treatment of PNI. The sciatic function index (SFI) test is a reliable accurate method for assessing sciatic nerve integrity after both partial disruption and regrowth.
RESUMO
Nicotine forms the major addictive component of the tobacco smoke. The pancreas is one of the organs where the metabolic processes of tobacco take place. This work was designed to study the effect of nicotine administration and the effect of its withdrawal on the pancreas of albino rat. Twenty-five male albino rats were separated into two groups. Group I acted as control. Rats in group II received 1.5 mg/kg body weight of nicotine by subcutaneous injection day after day divided into two subgroups, each one containing ten rats. The first one received treatment for 4 months, and then the rats were sacrificed, while the second group received treatment for 4 months, and the rats were sacrificed after one month from treatment stoppage. The pancreases were removed and processed for histological examination and electron microscopy. Histopathological and electron microscopic examination of the pancreas of nicotinetreated rats showed degenerated and distorted pancreatic acini and β cells. These changes included pyknotic nucleus, cytoplasmic swelling, vacuolization and interstitial edema in pancreatic acinar cells. Some of the islets of Langerhans showed vaculation inside their cell and others did not show apparent changes. There was also a significant decrease in lipase and glucose levels. However, after withdrawal of nicotine, the pancreas showed more degenerated pancreatic acini and β cells. There was significant increase in blood glucose level and significant decrease in lipase of treated rats. Nicotine treatment for four months induced histopathological changes in both exocrine and endocrine pancreatic tissue that resemble the picture of chronic pancreatitis. These changes persisted long after cessation of nicotine exposure
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