Effects of Calendula officinalis extract on liver histopathology, lipid profile, and oxidative stress in rats submitted to a diet rich in cholesterol and carbohydrates.

PURPOSE: To evaluate the modulatory properties of Calendula officinalis L. (Asteraceae) (C. officinalis) extract on cafeteria diet-fed rats. METHODS: A cafeteria diet was administered ad libitum for 45 days to induce dyslipidemia. Then, the rats were treated with the formulations containing C. officinalis in the doses of 50, 100, and 150 mg/kg or only with the vehicle formulation; the control group received a commercial ration. RESULTS: The cafeteria diet decreased glutathione S-transferase activity and high-density lipoprotein plasmatic levels and damaged the hepatic architecture. The C. officinalis extract was able to reduce lipid infiltration in liver tissue and to modulate oxidative stress and lipid profile markers. CONCLUSIONS: The correlations between the variables suggest a pathological connection between oxidative stress markers and serum lipid profile.

Effects of Calendula officinalis extract on liver histopathology, lipid profile, and oxidative stress in rats submitted to a diet rich in cholesterol and carbohydrates

Purpose: To evaluate the modulatory properties of Calendula officinalis L. (Asteraceae) (C. officinalis) extract on cafeteria diet-fed rats. Methods: A cafeteria diet was administered ad libitum for 45 days to induce dyslipidemia. Then, the rats were treated with the formulations containing C. officinalis in the doses of 50, 100, and 150 mg/kg or only with the vehicle formulation; the control group received a commercial ration. Results: The cafeteria diet decreased glutathione S-transferase activity and high-density lipoprotein plasmatic levels and damaged the hepatic architecture. The C. officinalis extract was able to reduce lipid infiltration in liver tissue and to modulate oxidative stress and lipid profile markers. Conclusions: The correlations between the variables suggest a pathological connection between oxidative stress markers and serum lipid profile.

Efeitos de um salgante isento de sódio sobre marcadores sanguíneos bioquímicos hepáticos, renais e cardíacos de ratos normo e hipertensos / Effects of a sodium-free salting agent on blood hepatic, renal and cardiac biochemical markers of normal and hypertensive rats

Introdução: A hipertensão arterial é um dos fatores de risco para doenças cardiovasculares, estando diretamente associada ao elevado consumo de sódio. Objetivo: Avaliar os níveis de marcadores de lesão hepática, renal e cardíaca em ratos hipertensos comparados aos seus controles normotensos, tratados com um salgante isento de sódio, água ou NaCl. Métodos: Ratos hipertensos (SHR) e seus controles normotensos (NWR) foram divididos em 3 grupos (n=7): G1 (água); G2 (solução aquosa contendo NaCl 70 mg/kg/dia); G3 (solução aquosa contendo salgante sem sódio 70 mg/kg/dia). Após 30 dias, o sangue dos animais foi processado. Resultados: Não houve diferença entre os níveis séricos de creatina quinase total, creatina quinase-MB, lactato desidrogenase, ácido úrico, aspartato aminotransferase e fosfatase alcalina tanto nos NWR como nos SHR tratados com NaCl ou Salgante. Houve diminuição da creatinina nos NWR e SHR tratados com NaCl e Salgante em relação aos controles (p<0,005). Conclusões: A suplementação diária com o Salgante e NaCl diminuiu os níveis séricos de creatinina nos grupos NWR e SHR. Contudo, não houve modificação nos níveis séricos de marcadores de lesão cardíaca e hepática. (AU)

Introduction: Hypertension is one of the risk factors for cardiovascular diseases, being directly associated with high consumption of sodium. Objective: To assess the levels of hepatic, renal and cardiac injury markers in hypertensive rats compared to their normotensive controls, treated with a salt free saline solution, water or NaCl. Methods: Hypertensive rats (SHR) and their normotensive controls (NWR) were divided into 3 groups (n = 7): G1 (water); G2 (aqueous solution containing NaCl 70 mg / kg / day); G3 (sodium salt-free aqueous solution 70 mg / kg / day). After 30 days, the animals' blood was processed. Results: There was no difference between serum levels of total creatine kinase, creatine kinase-MB, lactate dehydrogenase, uric acid, aspartate aminotransferase and alkaline phosphatase in both NWR and SHR1 treated NaCl or Salgante. There was a decrease in creatinine in NWR and SHR treated with NaCl and Salgante comparing to controls (p <0.005). Conclusions: Daily supplementation with sodium salt-free aqueous solution and NaCl decreases serum creatinine levels in NWR and SHR groups. However, there was no change in serum levels of cardiac and hepatic injury markers. (AU)

Chronic treatment with red wine modulates the purinergic neurotransmission and decreases blood pressure in hypertensive SHR and diabetic-STZ rats.

It is known that red wine has cardioprotective properties. However, its influence is unknown about purinergic system. Therefore, we study the influence of the treatment with red wine or ethanol in purinergic neurotransmission. We used Wistar Kyoto rats (WKY), diabetic streptozotocin-induced WKY and spontaneously hypertensive rats (SHR), treated with red wine (12.5%) or ethanol (12.5%). The cardiovascular function stimulated with purinergic agonists and systolic blood pressure (SBP) was assessed. In atria of diabetics and SHRs, the P1 receptor response was decreased, unlike the P2 receptor response was increased. Likewise, in aorta the affinity to adenosine (ADO) was decreased from SHRs and diabetics. Furthermore, the P2X function was increased just SHRs. All these alterations were improved after treatment with red wine, resulting in reduction of SBP from diabetics and SHRs, but not when treated with ethanol. This study has important implications, because it is shown that consumption of red wine can improve cardiovascular system by purinergic neurotransmission.

Time-dependent up-regulation of Ca(2+) channels in vas deferens of newborn rats fed with breast milk of mothers under treatment with nifedipine.

Our aim was to check for calcium channel maturation and regulation on newborn rats during breastfeeding by mothers treated with the L-type calcium channel blocker nifedipine. Contractions by KCl and radioligand binding techniques were used to verify if Ca(2+) channels are modified in rat vas deferens of 40-day old litters that were breastfed by mothers injected daily with nifedipine during nursery. Injections were applied in the beginning (1st until 8th day), middle (9th until 16th day), or end (17th until 24th day) of nursery, to verify the period of highest susceptibility of newborn to nifedipine receptor regulation. Contractile responses revealed that only after the middle period of treatment of mothers the maximal effects (E(max)) induced in pups by KCl were increased by about 35%, without changes of apparent affinity (pD(2)). Additionally, binding studies with [(3)H] Isradipine in cell membrane preparations showed a greater density (B(max)) of Ca(2+) channels by about 55%, without changes of affinity (K(d)). Changes were not detected after treatment of mothers in the beginning or end of breastfeeding. In addition, in vas deferens of 60-day old litters, the E(max) returned to control values, showing that changes were not persistent. Moreover, body and vas deferens weights and blood testosterone of newborn were never changed. The histology of mammary gland was similar for treated and control mothers, suggesting a stable milk production. It is concluded that nifedipine treatment of mothers, if made during the 9th to 16th day of lactation, produced a short lasting reversible up-regulation of L-type Ca(2+) channels.

Up-regulation of Ca(2+) channels in vas deferens after chronic treatment of newborn rats with nifedipine.

Radioligand binding and contraction techniques were used to verify if L-type Ca(2+) channels are modified in rat vas deferens after treatment with the blocker nifedipine (15 microg), injected at 7, 14, 21 and 28 days after birth. Vas deferens tissue was used 10, 30 and 90 days after the last injection, to verify if modifications are persistent. Binding studies with cell membranes, using [(3)H]isradipine, showed an increase of the density (B(max)) of Ca(2+) channels by more than 60%, after 10 and 30 days, without changes of affinity (K(d)). Maximal contractions (E(max)) of KCl, were increased by 106% and 37%, respectively, after 10 and 30 days, without changes of apparent affinity (pD(2)). After 90 days, the values of B(max), K(d), E(max) and pD(2) were not different from the controls. Differences were also not found for rats injected when adult. It is concluded that treatment of newborn, but not of adult, rats with nifedipine produced a long-lasting, though reversible, up-regulation of L-type Ca(2+) channels.