Although studies have shown that ginger, as an herbal remedy and zinc are able to improve inflammation, oxidative stress, autophagy, and metabolism of lipid and glucose, their molecular mechanisms are unknown. Therefore, this study was aimed to examine the therapeutic effects of ginger with zinc supplement for eight weeks on fructose-induced metabolic syndrome (MS). Ninety-six adult male Sprague Dawley rats (220 g ± 20) were randomly assigned to twelve controlled and treated groups. After the last treatment session, the level of lipid profiles, glucose, insulin, and leptin as metabolic factors and liver enzymes as biomarkers to evaluate liver function in serum were measured. The level of antioxidant enzymes and lipid peroxidation to evaluate the oxidative status and the TNF-α level as a biomarker to assess the state of inflammation in liver were also measured. The level of zinc along with the expression of NF-κB, mTORC1, PPAR-α, SREBP-1c, and Nrf2 in liver was also evaluated. The level of metabolic factors and liver enzymes in serum along with lipid peroxidation and TNF-α in liver increased; zinc and antioxidant enzymes levels decreased in rats with MS compared to control rats (p < .05). The hepatic expression of SREBP-1c, NF-κB and mTORC1 were upregulated and the expression of PPAR-α and Nrf2 were downregulated in rats with MS compared to control rats (p < .05). Treatment with different doses of ginger, zinc, and the combination of them could improve metabolic, inflammatory oxidative stress factors, and expression of the above genes in rats with MS compared to the MS group (p < .05). It can be concluded that ginger, zinc, and the combination of them could improve oxidative damage, inflammation, and autophagy induced by fructose and could adjust the glucose and lipid metabolism and the homeostasis of zinc in rats with MS. Practical applications Due to the increasing prevalence of metabolic diseases, the use of plant compounds such as ginger has attracted widespread attention. Ginger as an herbal remedy with predominant pharmacological properties due to its availability, cheapness, and lack of side effects is also very popular for the treatment of metabolic disorders in folk How to cite this article:

ObjectivesThis study was conducted to evaluate the effect of eplerenone on the RAAS and kidney function in rats with thyroid hormone disorders.MethodsThis study involved 30 male Wistar albino rats, divided into three groups. The first group (N = 6) served as a control. The second group involved 12 rats with experimentally induced hypothyroidism through receiving propylthiouracil (0.05% w/v) in drinking water for one month, which was divided into two subgroups of six rats each. The first subgroup served as a positive hypothyroid control, and the second subgroup received oral daily dose of eplerenone (100 mg/kg) for 14 days. The third group included 12 rats with induced hyperthyroidism with L‐thyroxin (0.0012% w/v) in drinking water, and rats in this group were also divided into two subgroups. The first subgroup served as a positive hyperthyroid control, and the second subgroup received oral eplerenone 100 mg/kg.ResultsEplerenone indicated a significant increase in renin and angiotensin I from 184.09 pg/ml and 178.66 pg/ml to 603.31 pg/ml and 250.88 pg/ml, respectively, meanwhile, aldosterone indicated no significant changes after inducing hypothyroidism and eplerenone administration.The induction of hyperthyroidism led to a significant increase in angiotensin I from 248.84 pg/ml to 292.22 pg/ml. Oral administration of eplerenone for 14 days caused a significant increase aldosterone from 364.23 pg/ml to 497.02 pg/ml.ConclusionEplerenone significantly increased the serum renin and angiotensin I in hypothyroid and aldosterone and angiotensin I in hyperthyroid rats. Aldosterone in hypothyroid rats was not changed by eplerenone.

Background: The latest anti-diabetic medication sodium-glucose co-transporter inhibitor along with the lowering of blood glucose has a cardioprotective and reno-protective effect, it has the ability to reduce the development of heart failure and decrease hospitalization in heart failure subjects with and without diabetes. This study was conducted to evaluate the effect of sodium-glucose co-transporter inhibitor dapagliflozin alone and in combination with eplerenone on the aldosterone hormone in the treatment of rats with experimentally induced heart failure.Method: Thirty Wister rats were randomly divided into five groups each of six rats, the first group served as a control group. The heart failure model was induced experimentally by intraperitoneal injection of isoprenaline 5mg/kg/day for one week for the rest of the experimental rat groups. The second group was a positive control. The third, fourth, and fifth groups received oral daily doses of dapagliflozin 10 mg/kg/day, eplerenone 100 mg/kg/day, and dapagliflozin-eplerenone 10,100 mg/kg/day respectively for four weeks.Results: Induction of heart failure in rats has significantly raised circulating BNP, NT-Pro BNP, aldosterone, troponin I, serum urea, and creatinine. Rats treated with dapagliflozin showed statistically significant decreases in BNP, NT-Pro BNP, aldosterone, troponin I, blood urea nitrogen, and serum creatinine. Non significant changes are seen in decreasing mean blood pressure. Dapagliflozin-eplerenone administration produced a significant reduction in plasma aldosterone level, heart rate, and diastolic blood pressure.Conclusion: The study demonstrates the cardiovascular benefit of sodium-glucose co transporter inhibitor dapagliflozin in rats with experimentally induced heart failure, reducing the myocardial stretch indicates the prominent role of dapagliflozin in reducing the development of heart failure and decreasing cardiovascular complications in subjects with and without diabetes. Moreover, the impact of dapagliflozin on renal function further contributes to cardiovascular benefits by reducing volume overload and neurohormonal activation which are features of cardiorenal syndrome.