Spilanthes filicaulis (Schumach. & Thonn.) C.D. Adams leaves protects against streptozotocin-induced diabetic nephropathy.

BACKGROUND AND OBJECTIVE: Diabetic neuropathy (DN) is a complex type of diabetes. The underlying cause of diabetic nephropathy remains unclear and may be due to a variety of pathological conditions resulting in kidney failure. This study examines the protective effect of the methanolic extract of Spilanthes filicaulis leaves (MESFL) in fructose-fed streptozotocin (STZ)-induced diabetic nephropathy and the associated pathway. METHODS: Twenty-five rats were equally divided randomly into five categories: Control (C), diabetic control, diabetic + metformin (100 mg/kg), diabetic + MESFL 150 mg/kg bw, and diabetic + MESFL 300 mg/kg bw. After 15 days, the rats were evaluated for fasting blood glucose (FBG), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), urea, uric acid, serum creatinine, reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and lipid peroxidation (MDA). Gene expression levels of cyclic adenosine monophosphate (cAMP), protein kinase A (PKA), cAMP response element-binding (CREB), cFOS and the antiapoptotic protein Bcl-2 were examined. RESULTS: We observed that MESFL at 150 and 300 mg/kg bw significantly downregulated the protein expression of cAMP, PKA, CREB, and cFOS and upregulated the Bcl-2 gene, suggesting that the nephroprotective action of MESFL is due to the suppression of the cAMP/PKA/CREB/cFOS signaling pathway. In addition, MESFL increases SOD and CAT activities and GSH levels, reduces MDA levels, and reduces renal functional indices (ALP, urea, uric acid, and creatinine). CONCLUSION: Therefore, our results indicate that MESFL alleviates the development of diabetic nephropathy via suppression of the cAMP/PKA/CREB/cFOS pathways.

Combined Administration of l-Carnitine and Ascorbic Acid Ameliorates Cisplatin-Induced Nephrotoxicity in Rats.

OBJECTIVES: Cisplatin (CIS) is an effective antitumor drug. However, its clinical use is limited due to nephrotoxicity. l-Carnitine and vitamin C are both natural antioxidant that can be obtained from diets. This study investigated the effects of l-carnitine and/or vitamin C in rats against cisplatin-induced nephrotoxicity. METHODS: Twenty-five male Wistar rats were divided into 5 groups of 5 rats each. Group 1, normal control. Group 2, positive control, received cisplatin (10 mg/kg/day intraperitoneally [i.p.]) for 3 days. Groups 3, 4, and 5 received cisplatin for 3 days and thereafter l-carnitine (50 mg/kg/day), vitamin C (100 mg/kg/day), or their combination, respectively, for 28 days. At the end of the study, a biochemical study was carried out in which nephrotoxicity markers, electrolytes, hematological indices, oxidative stress biomarkers, and renal histopathological alterations were evaluated. RESULTS: CIS-treated rats developed significant polyuria, increase in the plasma levels of creatinine, urea, and inorganic phosphate (Pi), alteration in hematological parameters, and decrease in plasma levels of Na+, Cl-, K+, Ca2+, and Mg2+. Measurements of 24-hour urine output demonstrated markedly decreased creatinine and urea and increased Na+, Cl-, K+, Ca2+, and Mg2+ levels in the CIS-treated group, whereas Pi levels were not changed. It also caused significantly decreased catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH) levels in the rats' kidneys. Histopathological scores revealed renal tubular damage in CIS-treated rats. However, l-carnitine, vitamin C, or their combination significantly attenuated the alterations caused by CIS in the plasma and kidneys of the rats. CONCLUSION: l-Carnitine and vitamin C administration ameliorated CIS-induced nephrotoxicity due to their antioxidant and anti-inflammatory effects.

Sub-acute administration of lower doses of nicotine caused sex-dependent improvement of renal function in Wistar rats.

The adverse and beneficial health effects of nicotine (NIC), the major alkaloid found in cigarettes and tobacco, are controversial. Most studies on NIC have focused on its effects on cardiovascular and nervous functions. This study aimed at determining dose- and sex-specific effects of sub-acute (28 days) NIC administration on some indices of kidney function in Wistar rats. Forty rats (20 males and 20 females), 8-9 weeks old (each housed in separate metabolic cage), were used for this study such that graded doses of NIC (1, 2 and 4 mg/kg i.p. for 28 days) were administered to both sexes while each control received distilled water at 0.2 mL/100 g i.p. Blood was collected under ketamine anesthesia (10 mg/kg i.m) for analyses and results obtained were compared at p < 0.05. The result showed beneficial alterations in plasma and urine level of creatinine, urea and uric acid (p < 0.05) as well as plasma and urine electrolyte level (Na+ and K+) in both sexes (p < 0.05). Also, there was significant improvement in creatinine clearance (p < 0.05) with no appreciable difference in their histological examination. Although these beneficial effects were more pronounced in the female than in the male (p < 0.05), administration at the highest dose showed potentially deleterious alterations from normal beneficial trend (p < 0.05) in both sexes. It was concluded that sub-acute administration of lower doses of NIC improves kidney function of Wistar rats; an effect that was more pronounced in the females than their male counterparts.

Polyphenol-rich extract of Vernonia amygdalina (Del.) leaves ameliorated cadmium-induced alterations in feeding pattern and urine volume of male Wistar rats.

AIM: To determine the effects of polyphenol-rich extract of the leaves of Vernonia amygdalina (PEVA) on the feeding pattern of rats that were exposed to cadmium (Cd) toxicity. MATERIALS AND METHODS: Thirty male Wistar rats, weighing 160-180 g, were divided into 6 groups of 5 rats each as follows; Group 1 received distilled water orally (0.2 ml/100 g), daily, throughout the period of study. Group 2 received Cd alone (in the form of CdSO4) at 5 mg/kg/day via intraperitoneal route for 5 consecutive days. Group 3 were pre-treated with Cd as Group 2 and thereafter left untreated for a period of 4-week. After the oral lethal dose of PEVA was determined, Groups 4, 5, and 6 were pre-treated with Cd as Group 2 after which they received graded doses of PEVA at 100, 200 and 400 mg/kg/day (0.2 ml/100 g), respectively via oral route for 4 weeks. Blood samples were collected for some plasma biochemical assays while urine samples were collected using metabolic cages. RESULTS: PEVA administration significantly increased (P < 0.05) the body weight and feeding patterns that were significantly reduced (P < 0.05) by Cd toxicity. PEVA also significantly reinstated the plasma antioxidant status, as well as glucose and urine volume of the rats toward control values (P < 0.05). CONCLUSION: PEVA can be an herbal alternative in the treatment or management of subjects manifesting alterations in feeding pattern and urine volume that is Cd-induced.