Renal ischaemia/reperfusion (I/R) injury is a common problem that occurs when blood flow is interrupted to the kidney in case of kidney transplantation, aortic cross-clamping and shock with subsequent resuscitation. Renal I/R injury is a complex conditions which includes the onset of an inflammatory process, which is associated with impairment of concentrating ability of the kidney and impairment of solute transport. Characteristically, renal I/R injury is associated with marked reduction in the protein expression of renal aquaporins (AQPs) mainly (AQP1, AQP2 and AQP3), and solute transporters were observed in this condition and could account for the impaired urinary concentration that observed in this condition. Recently, many agents were tested for a possible protective effect against this insult such as erythropoietin (EPO), α-melanocyte-stimulating hormone (α-MSH) and α-lipoic acid which were proved to prevent downregulation of AQPs and solute transporters. The aim of this short review is to outline the potential pathophysiological role of AQPs in renal I/R injury and to put a spotlight on the modulation of renal functions impairment in renal ischaemia by new drugs that prevent downregulation of AQPs.
One of the most prevalent cardiovascular problems linked with type 2 diabetes mellitus (T2DM) is diabetic cardiomyopathy (DCM). DCM is associated with myocardial oxidative stress, inflammation, apoptosis, suppressed autophagy, extracellular matrix remodeling, and fibrosis. The current study aims to investigate the protective effect of sodium-glucose transport 2 inhibitor (SGLT2i) dapagliflozin and/or exercise on DCM. Thirty adult male Sprague Dawley rats are used. T2DM is induced by a 6-week high-fat diet (HFD) followed by a single intraperitoneal (IP) injection of 35 mg/kg streptozotocin (STZ). Rats are divided into five groups, control, diabetic (DM), DM + swimming, DM + dapagliflozin, and DM + dapagliflozin and swimming. Serum glucose, insulin, insulin resistance (HOMA-IR), and cardiac enzymes (CK-MB and lactate dehydrogenase (LDH) are measured. Heart specimens are used for evaluation of cellular oxidative stress markers malondialdehyde (MDA), antioxidant enzymes, glutathione (GSH), and catalase (CAT), as well as mRNA expression of TGF-β, MMP9, IL-1β, and TNF-α. Stained sections with haematoxylin and eosin (H & E) and Masson trichrome are used for histopathological evaluation and detection of fibrosis, respectively. Immunohistochemical staining for apoptosis (caspase-3), and autophagy (LC3) are also carried out. The combinations of SGLT2i and exercise exhibited the most significant cardioprotective effect. It improved diabetic-induced histopathological alterations in the myocardium and attenuated the elevation of serum blood glucose, CK-MB, LDH, myocardial MDA, and mRNA expression of TNF-α, IL-1β, TGF-β, MMP9, and the immune expression of caspase-3. Moreover, this combination increased the serum insulin, myocardial antioxidants GSH and CAT, and increase the immune expression of the LC-3. In conclusion, a combination of SGLT2i and exercise exerted a better antioxidant, anti-inflammatory, and antifibrotic effect in DCM. Moreover, the combination enhances the autophagic capacity of the heart.
Aspartame is a synthetic sweetener that is unlikely to have a negative impact on the cerebellar cortex. The current study was designed to evaluate the histopathological changes in the cerebellar cortex of aspartame-treated albino rats and the possibility of recovery from aspartame induced cerebellar injury. Three groups of six mature male albino rats, totaling 18, were allocated. Daily doses of distilled water were given to the control group. Group 2 (ASP group): received 250 mg/kg ASP by oral rote for 12 weeks. Group3 (Recovery) received 250 mg/kg/day aspartame for eight weeks, then a daily dosage of distilled water equal to the aspartame dose for the next 6 weeks. The rats were anesthetized, and their cerebella were dissected for immunohistochemical and histological studies. Studies in morphometry and statistics were carried out. Nitric oxide (NO), reduced glutathione (GSH), and malondialdehyde (MDA) levels were assessed in the cerebellum tissue. When compared to the control group, there was a very significant rise in MDA and NO levels and a reduction in GSH levels in the aspartame group. MDA and NO levels were decreased associated with a significant increase in GSH level compared to the aspartame group in the recovery group. Cerebellar cortex of aspartame group showed features of neurodegeneration, and apoptosis. The latter features were decreased in the recovery group. In conclusion, aspartame consumption has reversible deleterious effect on cerebellar cortex.
Background: the literature is controversial about influence of stress on body weight. Chronic stress can activate both orexogenic and anorexigenic pathways with subsequent increase or decrease in body weight. Mechanisms behind these changes still need further evaluations. Aim and objectives: in the present study effect of different chronic stressors on body weight of young and middle aged rats and associated changes in leptin level have been investigated. Results: Chronic stress both (noise and restraint stress) resulted in a significant decrease in weight gain in young rats but significant weight loss in middle aged rats. There was significant elevation of blood glucose level and lipid profile in all stressed groups as compared with control groups. Serum level of insulin, leptin, and HOMA index were significantly elevated in noise stress group but significantly reduced in restraint stress groups. Conclusion: chronic stress caused significant body weight changes that differ according to age of animal associated with metabolic changes that could result in many forms of metabolic syndrome as a result of impaired lipid and glucose metabolism. Keywords Stress Young and middle age Leptin Insulin Blood glucose Bull. of Egyp. Soc. Physiol. Sci.
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