The Impact of Procyanidin Extracted from Crataegus azarolus on Rats with Induced Heart Failure.

This study aimed to investigate the possible use of Procyanidin extracted from Crataegus azarolus in the treatment of induced heart failure in rats. Thirty-six male rats were randomly assigned to three groups; the first two groups had six rats each, and the third group included four subgroups (each with six rats). The first group was regarded as the control group, while the second group (normal rats) received oral Procyanidin 30mg/kg/day for 14 days. The rest of the experimental groups were all injected intraperitoneally with 5mg/kg/day for seven days to induce heart failure. The first subgroup (IIIa) served as a positive control, and the other subgroups (IIIb, c, and d) received oral Procyanidin 30mg/kg/day, spironolactone 20mg/kg/day, and digoxin 7Mcg/kg/day, respectively, for 14 days. Heart failure induction in rats significantly increased levels of cardiac biomarkers, including NT-proBNP, BNP, ALP, MMP9, CPK, systolic, and diastolic blood pressure. The normal rats that received only Procyanidin experienced a significant decrease in the ALP level. Moreover, Procyanidin, accompanied by spironolactone and digoxin, significantly decreased NT-proBNP, BNP, ALP, and diastolic BP in rats with heart failure. Procyanidin extracted from C. azarolus significantly decreased cardiac biomarkers in rats with iso-induced HF. The final results demonstrated similar effects with both spironolactone and digoxin in induced heart failure in rats, revealing the possibility of using Procyanidin in the HF treatment.

Re-tasking the use of pre-existing medications and potential therapeutic options for coronavirus disease (COVID-19): systematic review of clinical studies.

With the emergence of coronavirus disease 2019 (COVID-19) in late December 2019, many clinical studies on a group of the pre-existing medications have been conducted to treat this disease. The purpose of this review was to compile the clinical evidences on the use of the pre-existing medications and potential therapeutic options for the management of COVID-19. We reviewed the literature to highlight the clinical studies on the use of these medications to be available as a scientific overview for further perspectives. Inadequate clinical evidences are available to be affirmed for the repurposing of old medications, and large scale clinical studies are needed to be carried out to further confirm the use of these agents. The clinical use of these medications should be well explained and follow the framework of Monitored Emergency use of Unregistered Interventions (MEURI) of World Health Organization (WHO).

Assessment of Nitrofurantoin as an Experimental Intracanal Medicament in Endodontics.

Background and Objectives. Multiple antibacterial agents have been mixed and used as an intracanal medicament-like modified triple antibiotic paste (MTAP) to eliminate Enterococcus faecalis (EF), which has been most frequently identified in the cases of failed root canal treatment and periapical lesions. This study is aimed at using a single antibacterial agent, nitrofurantoin (Nit), as an experimental intracanal medicament paste against different clinical isolates of EF), which has been most frequently identified in the cases of failed root canal treatment and periapical lesions. This study is aimed at using a single antibacterial agent, nitrofurantoin (Nit), as an experimental intracanal medicament paste against different clinical isolates of Materials and Methods. Three strains of EF), which has been most frequently identified in the cases of failed root canal treatment and periapical lesions. This study is aimed at using a single antibacterial agent, nitrofurantoin (Nit), as an experimental intracanal medicament paste against different clinical isolates of n = 90), group M (MTAP) (n = 90), group M (MTAP) (n = 90), group M (MTAP) (EF), which has been most frequently identified in the cases of failed root canal treatment and periapical lesions. This study is aimed at using a single antibacterial agent, nitrofurantoin (Nit), as an experimental intracanal medicament paste against different clinical isolates of n = 90), group M (MTAP) (n = 90), group M (MTAP) (n = 90), group M (MTAP) (EF), which has been most frequently identified in the cases of failed root canal treatment and periapical lesions. This study is aimed at using a single antibacterial agent, nitrofurantoin (Nit), as an experimental intracanal medicament paste against different clinical isolates of. RESULTS: Nit could eradicate S1, S2, and S3 completely with concentrations of 6.25, 12.5, and 25 mg/mL, respectively, while MTAP showed complete eradication of the three strains only at 25 mg/mL. In all the groups, it was found that the CFU counts of EF), which has been most frequently identified in the cases of failed root canal treatment and periapical lesions. This study is aimed at using a single antibacterial agent, nitrofurantoin (Nit), as an experimental intracanal medicament paste against different clinical isolates of. CONCLUSION: At the concentration of 25 mg/mL, the Nit paste is effective in eradicating EF completely when it is used as an intracanal medicament.EF), which has been most frequently identified in the cases of failed root canal treatment and periapical lesions. This study is aimed at using a single antibacterial agent, nitrofurantoin (Nit), as an experimental intracanal medicament paste against different clinical isolates of.

The effect of eplerenone on the renin-angiotensin-aldosterone system of rats with thyroid dysfunction.

OBJECTIVES: This study was conducted to evaluate the effect of eplerenone on the RAAS and kidney function in rats with thyroid hormone disorders. METHODS: This 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. RESULTS: Eplerenone 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. CONCLUSION: Eplerenone 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.

Aliskiren, Fosinopril, and Their Outcome on Renin-Angiotensin-Aldosterone System (RAAS) in Rats with Thyroid Dysfunction.

BACKGROUND AND OBJECTIVES: Thyroid hormones have an important role in the growth and development of various tissues including the kidney, which is the major site of renin release and the consequent angiotensin and aldosterone formation. Therefore any derangement in thyroid function can result in abnormal functioning in the renin-angiotensin-aldosterone system. The current study was undertaken to find the impact of using a direct renin inhibitor (Aliskiren) and an angiotensin-converting enzyme inhibitor (Fosinopril) on the components of the renin-angiotensin-aldosterone system (RAAS) in rats with thyroid dysfunctions. METHOD: Forty-two male albino rats were divided into three subgroups. First group (6 rats) served as control. Second group (18 rats) served as hyperthyroid group (6 rats positive control, 6 rats given Aliskiren, and 6 rats given Fosinopril). Third group (18 rats) served as hypothyroid group (6 rats positive control, 6 rats given Aliskiren, and 6 rats given Fosinopril). Induction of hyperthyroidism and hypothyroidism was done through daily oral administration of L-Thyroxine and Propylthiouracil, respectively. On day 40 of the study, the rats were sacrificed and blood was collected for estimation of renin, angiotensin I, angiotensin II, aldosterone, TSH, T3, and T4. The collected blood samples were also used for estimation of levels blood urea, serum creatinine, liver enzymes, and serum electrolytes. Blood pressure and urine collection were done on days 1 and 40. The collected urine was used for estimation of urine flow, sodium excretion, and potassium excretion rates. RESULTS: In hypothyroid induced rats, serum renin level dropped as expected, while the use of Aliskiren and Fosinopril on these hypothyroid rats raised renin level due to the feedback mechanism. Both angiotensin I and II were significantly (P <0.05) lower than normal levels in the hypothyroid rats, unlike the level of aldosterone, which was higher than normal level. There was nonsignificant lowering in BP (systolic, diastolic, and mean BP) in the hypothyroid rats. Treatment of these rats with Aliskiren and Fosinopril did not lower the blood pressure more than normal when compared to the hypothyroid group. The hypothyroid rats also showed a decrease in level of serum creatinine. In hyperthyroid rats, there was a rise in levels of serum renin, angiotensin II, and aldosterone; nevertheless, the increase in angiotensin I level was significant. The use of Aliskiren and Fosinopril increased the level of renin nonsignificantly (decreased angiotensin I significantly). Hyperthyroid rats showed a significant increase in systolic, diastolic, and mean blood pressure. Both Aliskiren and Fosinopril increased urine flow, Na+ excretion, and K+ excretion rates. Aliskiren was better at reducing the high blood pressure. CONCLUSION: Aliskiren and Fosinopril in hyperthyroid rats decreased serum angiotensin I, angiotensin II, and aldosterone. Blockade of renin and inhibition of angiotensin-converting enzyme both resulted in a rebound increase in level of renin in hypothyroid rats. Aliskiren is better at controlling blood pressure in hyperthyroid rats. Urine flow, sodium excretion, and potassium excretion rates were improved by the use of Aliskiren and Fosinopril in hyperthyroid rats.

Effects of neprilysin-renin inhibition in comparison with neprilysin-angiotensin inhibition on the neurohumoral changes in rats with heart failure.

BACKGROUND: The activation of neurohumoral compensatory mechanisms is a common physiological phenomenon in heart failure in order to make up for a failing heart, which will usually have a deteriorating effect on overall health condition. Many medications, such as neprilysin and angiotensin inhibitors, have recently been introduced to remediate neurohumoral changes. This study was conducted to evaluate the efficacy of the sacubitril-aliskiren combination versus the sacubitril-ramipril combination in the treatment of neurohumoral changes in rats with experimentally induced heart failure. METHOD: Thirty Wister rats were randomly assigned into five groups each of six rats, the first group was the control group. Intraperitoneal isoprenaline injections of 5 mg/kg/day for 1 week were used to induce experimental models of heart failure in rats of the rest of experimental groups. The second group served as a positive control. Rats in the third, fourth, and fifth groups received oral daily dose of sacubitril 30 mg/kg/day, sacubitril-aliskiren 30,10 mg/kg/day, and sacubitril-ramipril 30/10 mg/kg/day respectively, for 2 weeks. RESULTS: Induction of heart failure in rats has significantly increased circulating NT-proBNP (980 ± 116.71 pg/ml), MMP9 (15.85 ± 0.57 ng/ml), troponin-I (3.09 ± 0.147 ng/ml), CK-MB (31.55 ± 1.69 ng/ml), renin (736 ± 45.8 pg/ml), urea (52.1 ± 1.57 mg/dl), and creatinine (0.92 ± 0.04 mg/dl). Significant decreases in glomerular filtration rate (7.031 ± 1.6 ml/hr./kg), urine flow (0.2761 ± 0.06 ml/h/kg), total solute excretion (0.11 ± 0.03 meq/m), and mean blood pressure (83.5 ± 2.6 mm hg) were seen in rats with heart failure. Rats treated with sacubitril combined with aliskiren or ramipril showed a statistically significant reduction of NT-proBNP, MMP9, troponin serum urea, and serum creatinine. Sacubitril-aliskiren or sacubitril-ramipril administration produced a significant increase in renin plasma level, total solute excretion, urine flow, and glomerular filtration rate. CONCLUSION: Sacubitril in combination with aliskiren or with ramipril effectively reduced plasma cardiac biomarkers, such as CK-MB, MMP9, and NT-proBNP, in rats with heart failure. Both combinations showed significant remediation of renal function through increasing GFR, urine flow, and total solute excretion, as well as reducing plasma level of renin. Net results revealed that the sacubitril-aliskiren combination has similar remediating effects on neurohumoral changes compared to the sacubitril-ramipril combination.