Abstract. Noise pollution has been realized as an environmental stressor associated with modern life style that affects our health without being consciously aware of it. The present study investigated the effect of acute, chronic intermittent and chronic continuous exposure to noise of intensity 80-100 dB on heart rate and mean systemic arterial blood pressure in rats and the possible underlying mechanisms. Noise stress causes significant increase in heart rate, mean systemic arterial blood pressure as well as significant increase in plasma levels of corticosterone, adrenaline, noradrenaline, endothelin-1, nitric oxide and malondialdehyde with significant decrease in superoxide dismutase and these values are significantly more worse in chronic continuous exposure to noise than acute or chronic intermittent exposure. These findings suggest that noise stress has many adverse effects on cardiovascular system via increasing plasma levels of stress hormones, oxidative stress and endothelial dysfunction. These findings have major implication in the management of adverse cardiovascular reactions of people subjected to daily noise stress.

Vancomycin-induced nephrotoxicity has been reported to occur in 5%-25% of patients who were administered with it. Several natural antioxidants were found to be effective against drug-induced toxicity. We evaluated the possible protective effects of spirulina and pycnogenol alone or in combination on vancomycin-induced renal cortical oxidative stress. Forty-nine rats were randomly divided into 7 groups: group I, control; group II, received spirulina 1000 mg/kg per day; group III, received pycnogenol 200 mg/kg per day; group IV, received vancomycin 200 mg/kg per day every 12 h; group V, (spirulina + vancomycin); group VI, (pycnogenol + vancomycin); and group VII, (pycnogenol + spirulina + vancomycin). At the end of the experiment, kidney functions were estimated and then the kidneys were removed, weighed, and sampled for histopathological, immunohistochemistry, and biochemical studies. Administration of spirulina and pycnogenol alone or in combination decreased elevated serum creatinine, blood urea nitrogen, renal malondialdehyde, and immunoexpression of the proapoptotic protein (Bax), autophagic marker protein (LC3/B), and inducible nitric oxide synthase induced by vancomycin. They increased reduced glutathione, glutathione peroxidase, superoxide dismutase, and immunoexpression of the antiapoptotic protein (Bcl2). They also ameliorated the morphological changes induced by vancomycin. The combination therapy of spirulina and pycnogenol showed better protective effects than the corresponding monotherapy.

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Background: Diabetic nephropathy is a major microvascular complication of diabetes and a primary cause of end-stage renal disease worldwide. This study was designed to assess whether control of hyperglycemia with empagliflozin, a new sodium glucose cotransporter (SGLT) 2 inhibitor could improve the renal functions in streptozotocin induced diabetic rats. Thirty two adult male albino rats were randomly assigned into four equal groups. Group I; non diabetic control, Group II; non diabetic rats treated with empagliflozin, group III; diabetic rats and group IV; diabetic rats treated with empagliflozin. Diabetic rats treated with empagliflozin showed significant increase in body weight and significant reduction in Kidney weight, blood glucose and glycated haemoglobin (HbA1c) levels. Empagliflozin also produced significant decrease in blood urea nitrogen (BUN), serum creatinine, urinary albumin excretion (UAE), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6) and transforming growth factor beta-1 (TGF-β1). It also attenuated Kidney tissue oxidative stress. Empagliflozin showed a renoprotective effect in streptozotocin induced diabetic rats through its glucose lowering effect and by reducing oxidative stress, inflammation, fibrosis and histopathological alterations. SGLT-2 inhibitor seems to be a promising therapeutic strategy for managing diabetes mellitus to slow the progression of diabetic nephropathy.

Osteoporosis is one of the most prevalent bone diseases especially among postmenopausal women. This study was conducted on 36 female rats divided into three equal groups; i) Sham-operated, ii) Ovariectomized (OVX), iii) Leptin treated ovariectomized group. At the end of experiment, blood was collected for measurement of serum alkaline phosphate (ALP), calcium (Ca), phosphorus (P), osteocalcin, receptor activator of nuclear factor κB ligand (RANKL) and osteoprotegerin (OPG). Urine was collected for measurement of urinary deoxypyridoline/creatinine (DPY/Cr). After eight weeks of treatment, administration of leptin inhibited OVX-induced weight gain with uterotrophic effect, decreased bone turnover markers (urinary DPY/Cr, serum osteocalcin and serum ALP) and serum RANKL while it resulted in significant increase in serum calcium and OPG. Moreover, it markedly decreased expression of RANKL and increased expression of OPG in proximal femur, and thus lowered the RANKL/OPG ratio. These findings suggests that the anti-osteoporotic effect of leptin was by inhibiting osteoclastogenesis via modulating RANKL/OPG ratio. Leptin had potential to be developed as alternative therapeutic agents of osteoporosis induced by postmenopause. Keywords • Leptin • Osteoporosis • Bone markers • RANKL • OPG • Osteoclastogenesis Bull. of Egyp. Soc. Physiol. Sci.