جستجوی مقالات مرتبط با کلیدواژه « Carvedilol » در نشریات گروه « پزشکی »

Today, it has been shown that it is possible for right ventricular (RV) wall motion abnormalities or RV functional disorders to occur during cancer treatment. Now, considering the effect of carvedilol on beta 1, 2, and alpha receptors and its antioxidant properties, it seems that it can prevent RV abnormalities. Therefore, the aim of this study was to investigate the possible protective effects of carvedilol in preventing RV dysfunction in patients with breast cancer treated with anthracyclines.

The present single‑blind clinical trial study was performed on 23 patients with breast cancer that 12 of them received only the anthracycline antineoplastic doxorubicin (Adriamycin®) chemotherapy (control group) and 11 patients received carvedilol in addition to anthracycline. To evaluate the effect of carvedilol, patients underwent transthoracic echocardiography before intervention and 2 weeks after the end of treatment with anthracyclines.

The two parameters of RV ejection fraction and RV fractional area change in the carvedilol group with a mean of 66.41% ± 8.10% and 51.85% ± 6.89% were slightly higher than the control group with a mean of 64.58% ± 6.83% and 50.48 ± 5.79%, respectively, which was not statistically significant (P > 0.05). In contrast, RV S wave tissue Doppler imaging (S‑TDI) in the control group with a mean of 0.13 ± 0.02 m/s was significantly lower than the carvedilol group with a mean of 0.14 ± 0.02 m/s (P = 0.022).

According to the results of the present study, the effect of using carvedilol as a preservative on improving RV function was seen compared to the control group, although this difference was not statistically significant.

The study was aimed at validating a si mple, rapid, and low-cost LC-MS/MS method for carvedilol and 4 / -hydroxyphenyl carvedilol assay in human plasma. The validated method was applied to investigate the pharmacokinetics after a low dose of 6.25 mg. carvedilol.

In this study, the plasma was extracted by liquid-liquid extraction and evaporated the organic layer to dryness, then both analytes in the residue were reconstituted and detected by LC- MS/MS. The method was validated following the guideline on bioanalytical method validation. Thirty-one healthy volunteers participated in the pharmacokinetic study. After 10 h of fasting, each volunteer received one tablet of 6.25 mg carvedilol orally. Blood samples were collected at 16 prescheduled time points. The plasma samples were analyzed for pharmacokinetics.

The method was linear over a range of 0. 050-50.049 ng/mL for carvedilol and 0.050- 10.017 ng/mL for 4 / -hydroxyphenyl carvedilol. Crucial validated results reached the requirements of selectivity, accuracy, precision, and stability. Pharmacokinetics of carvedilol and 4 / -hydroxyphenyl carvedilol were evaluated which showed C max at 21.26 ± 9.23 and 2.42 ± 2.07 ng/mL; AUC 0-t 66.95 ± 29.45 and 5.93 ± 3.51 ng.h/mL; AUC0-inf 68.54 ± 30.11 and 6.78 ± 3.49 ng.h/mL; and T 1/2 6.30 ± 1.95 and 6.31 ± 6.45 h, respectively.

 The validated method was able to detect and quantify both analytes in plasma samples and can be applied to the pharmacokinetic study of carvedilol and 4/ -hydroxyphenyl carvedilol after receiving carvedilol at 6.25 mg orally.

The present study mainly aimed to prepare solid dispersions (SDs) of a poorly water-soluble compound, carvedilol (CA), in the presence of pluronic F68 (F68) and myrj 52 by adopting wet milling technique in order to enhance drug dissolution. The process enabled the preparation of SDs without using any toxic organic solvents. SDs with different CA, surfactant ratios were prepared by adopting wet milling followed by freeze-drying method and evaluated for their particle size and dissolution. They were also characterized based on/using X-ray diffraction (XRD), differential scanning calorimetry (DSC), fourier transform infrared (FTIR) spectroscopy, scanning electron microscope (SEM), and saturated solubility. The effect of cryoprotectant type on the dissolution and particle size of SDs was also investigated. Wet milling process resulted in the reduced particle size depending on the type of surfactant. The significant drug dissolution and saturated solubility enhancement were recorded for milled SD formulations. In this regard, Myrj had a greater impact compared to F68. Dissolution efficiencies (DE30) obtained for the myrj-included SDs were up to 8.2-fold higher than that of untreated CA. The type of cryoprotectant was also found to affect the drug dissolution. According to the results, partial amorphization occurred in wet-milled samples, as confirmed by XRD and DSC analysis. It was concluded that using an appropriate surfactant along with wet-milling method may have been an effective approach for improving the dissolution rate of CA, a poorly soluble compound.

Acrylamide is a potent neurotoxic compound and has harmful effects on brain cells. Acrylamide promotes oxidative, inflammatory, and apoptotic mediators in the CNS leading to neurological disorders. The goal of the current study was to examine the potential protective effect of carvedilol and its underlying mechanisms in a mouse model of acrylamide-induced brain injury.  Mice were treated with acrylamide (50 mg/kg/day, IP) and carvedilol (5 and 10 mg/kg/day, oral) for 11 continuous days. At the end of the experiment, mice were subjected to gait assessment. They were sacrificed and brain tissues were collected for histological and biochemical analysis.  The results showed that treatment of mice with carvedilol decreased acrylamide-induced bodyweight loss, abnormal gait, and histopathological damage in the brain tissue. Carvedilol treatment significantly reduced the levels of malondialdehyde (MDA) and carbonyl protein and increased the levels of glutathione (GSH), catalase, superoxide dismutase (SOD), nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1). Carvedilol treatment also decreased myeloperoxidase (MPO) activity, expression of nuclear factor kappa B (NF-κB), inducible nitric oxide synthase (iNOS), overproduction of nitric oxide (NO) and proinflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in the brain of mice exposed to acrylamide. Furthermore, administration of carvedilol significantly decreased the levels of bax, cytochrome-c, and caspase-3 as markers of apoptosis in acrylamide-treated mice.  These findings indicate that carvedilol is able to attenuate acrylamide-induced damage to the CNS by inhibition of oxidative stress, inflammation, and apoptosis.

Most people with diabetes suffer from cardiovascular problems; however, increased oxidative stress caused by diabetes can increase the risk of DNA damage and cancer. Carvedilol is a third-generation beta-blocker that can both improve heart function and prevent oxidative stress.

The present study aimed to assess carvedilol’s genoprotective effects against hyperinsulinemia-induced DNA strand break in rats.

To evaluate the extent of DNA damage caused by high insulin concentrations and the effect of carvedilol on these lesions, isolated lymphocytes of high-fat type 2 diabetic rats were evaluated using the comet method.

Our results in this study using the comet method showed that hyperinsulinemia and hyperglycemia of high-fat diet have significant genotoxic parameters in rats (tail length 84.35 ± 0.23 vs. 0.90 ± 0.02, % DNA in tail 16.09 ± 0.09 vs. 7.63 ± 0.04, and tail moment 13.58 ± 0.09 vs. 0.07 ± 0.01) compared with the control group (P < 0.001). In rats receiving carvedilol, we observed the genoprotective effect in a dose-dependent manner, which is predicted due to the antioxidant activity of carvedilol and its metabolites.

It does not have an adverse effect on the blood sugar profile of diabetics and reduction of cardiovascular complications of the disease; carvedilol can prevent genetic damage and cancer risk in hyperinsulinemia induced by the high-fat diet.

Trastuzumab is an efficient monoclonal antibody used in the treatment of Her2-positive breast cancer. Despite its prominent effect on Her2-positive patients’ disease-free Survival. Trastuzumab-induced cardiotoxicity is still one of the main challenges.  Angiotensin-converting enzyme inhibitors (ACE inhibitors) are one of the most potent agents used in heart failure, which also showed confirmed cardioprotective effects against anthracycline and doxorubicin. We aimed to assess the cardioprotective effects of Carvedilol in a randomized clinical trial study.

sixty non-metastatic Her-2 positive patients (30 cases; 30 controls) were entered to the study via a simple randomization method. Carvedilol was administered for the patients with the starting dose of 3.125 mg twice a day and started 7 days before trastuzumab administration. The dose has been increased in a three-week period to reach 12.5 mg twice a day and continued until the end of therapy. All the patients underwent an echocardiography after receiving Adriamycin and Cyclophosphamide in order to measure basal Ejection Fraction (EF) and Pulmonary Artery Pressure (PAP). Each patient underwent a follow-up echocardiography in 3,6,9 and 12 months after initiation of the treatment. Finally, all the patients went through the last episode of echocardiography 1 month after the end of treatment. All the Measured PAP and EF has been recorded and analyzed

EF and PAP changes for both groups had no significant changes during the course of treatment with Trastuzmab (p-value = 0.628 and p-value = 0.723, respectively). 7 patients in the intervention group and 2 patients in the control group presented with EF decrease. Also, 8 patients in the intervention and 9 patients in the control groups showed PAP increase.

According to our results, in patients with HER2-positive breast cancer treated with trastuzumab, Carvedilol showed no significant protective effect on trastuzumab-induced cardiotoxicity.

The present study aims to assess and compare the effects of carvedilol and terazosin plus enalapril on lower urinary tract symptoms (LUTS), urine flow, and blood pressure (BP) in patients with moderate hypertension (HTN) and benign prostatic hyperplasia (BPH).

In this randomized crossover trial, a total of 40 men with HTN and LUTS symptoms were enrolled. The first group was treated with carvedilol, and the second group received terazosin plus enalapril. After eight weeks of treatment, the patients experienced a one-month washout period, and the treatments changed and were continued for eight weeks. To diagnose BPH in the study, the international prostate symptom score (IPSS) questionnaire was used. Moreover, the prostate-specific antigen (PSA), the post-void residual (PVR) urine volume, and the maximum urinary flow rate (Q-max using the uroflowmetry test) were measured.

Effect assessment results in this crossover trial illustrated neither carryover effects nor significant treat-ment effects on all primary outcomes (P > 0.05). Moreover, the results for the period effect indicated a significant reduction in BP (systolic and diastolic), PVR, and IPSS, yet a significant raise in Qmax.

The effects of carvedilol are similar to those of the combination of terazosin and enalapril in patients with moderate HTN and BPH in controlling LUTS. Carvedilol could be used as an appropriative drug in patients with moderate HTN and cardiac problems with LUTS of BPH. Further studies are recommended to be conducted to investigate and compare the efficacy of carvedilol with that of other alpha-blockers with a larger sample size and over a longer period of time

 To assess the association between hepatic venous pressure gradient (HVPG) baseline and the response rate of cirrhotic in patients who received carvedilol treatment.

 In total 48 cirrhotic patients with a basic HVPG value greater than 12 mmHg were included (from July 2011 to October 2014). All patients received carvedilol treatment and underwent the second HVPG measurement 7 days later. In the following, all participants received an endoscopic variceal ligation (EVL) treatment.

 HVPG was significantly reduced from 16.04 ± 3.10 to 12.76 ± 5.26 mmHg following carvedilol treatment. The response rate was about 58.33% (28/48). The response rate of the HVPG < 16 mmHg group (71.4%) was significantly higher than that of the HVPG ≥ 16 mmHg group (40%) (P < 0.05). Patients were followed up for a median of 26 months, ranged from 6 to 33 months. During the follow-up period (two years), the rebleeding rate was 9.97% and 49.56% in HVPG < 16 and HVPG ≥ 16 mmHg groups, respectively, with a statistically significant difference (P = 0.004). Also, the mortality rate (at 2 years) was 5.26% and 21.05%, respectively, which was significant (P = 0.035).

 This study demonstrated that the response rate of carvedilol on portal hypertension may be affected by the HVPG baseline, and the carvedilol was effective in reducing HVPG, especially for those with a HVPG < 16 mmHg.

Statins frequently cause myopathy especially in combination with fibrates, and physical activity is considered a trigger for the muscle disorder. Elevated plasma levels of creatine kinase (CK), lactate dehydrogenase (LDH) and aldolase, are the main indicators of the severity of myopathy. Carvedilol is commonly used with lipid-lowering drugs in the management of heart failure, hypertension and dyslipidemia. It is not yet clear whether carvedilol, an alpha and β blocker, and anti-oxidant, may influence the development of myopathy when combined with statins and fibrates in cardiac patients. 

In this animal experiment, a 10 days regimen containing oral atorvastatin and gemfibrozil at doses of 80 and 1000 mg/kg/day, respectively, was used to induce myopathy in rats. The animals were forced to swim in a pool on days 8, 9 and 10 into the study. Carvedilol (2.5 mg/kg/day) was added to atorvastatin and gemfibrozil during the 10-day study period, in addition to the exercise protocol given to the treatment groups only. The mean of swimming tolerance times and the serum levels of CK, LDH and aldolase were measured at the completion of the study. 

Carvedilol did not significantly alter the swimming tolerance time or the plasma levels of CK, LDH and aldolase in the rats receiving ATV, GMF and carvedilol plus the exercise protocol, compared with those that did not receive carvedilol (P>0.05).

Carvedilol may be used in combination with lipid-lowering drug in the management of patients with heart failure and hypertension, pending its safety approval by clinical studies in humans.

Carvedilol, the third generation of vasodilators; serves as the blocker of non-selective beta-adrenergic receptor and alpha1 adrenergic receptor. It could protect the cardiovascular system of patients receiving dialysis treatment. However, current clinical trials discussing the therapeutic benefit of carvedilol on patients receiving dialysis treatment remain inconsistent. Consequently, we decided to perform a meta-analysis to evaluate the clinical efficacy of carvedilol on patients receiving dialysis treatment. A search was conducted using EMBASE, Pubmed, Cochrane Central Register of Controlled Trials, Wanfang database, Chinese National Knowledge Infrastructure (CNKI), and VIP information database up to February 2020. We research publications (include English and Chinese language) that discuss the effects of carvedilol on cardiovascular events, all-cause mortality, hospitalizations or left ventricular ejection fraction (LVEF) in dialysis population. Our analysis included 4 randomized control trials and 2 observational studies. We discussed the therapeutical effects of carvedilol on all-cause mortality, cardiovascular events, hospitalizations, and LVEF of patients receiving dialysis treatment. Totally, this analysis reported 2998 hemodialysis (HD) patients. We found a significant association between carvedilol and reduced incidence of all-cause mortality, cardiovascular events and hospitalizations in HD patients. In addition, carvedilol significantly improves LVEF (n = 241; WMD = 6.95; 95% CI, 0.54 to 13.36; I2 = 90%) in HD population. Our systematic review and meta-analysis demonstrates that carvedilol is associated with a reduced incidence of cardiovascular events, all-cause mortality and hospitalizations in patients on HD. Besides; carvedilol significantly improves LVEF in HD population. Nevertheless, high-quality and well-powered evidence is still needed, so as to further confirm the impacts of carvedilol on HD patients.

The present work is aimed to study the effect of different parameters on the fluorescence intensity of atenolol (ATE) and carvedilol (CAR) and optimization by response surface methodology (RSM) to provide a simple analytical method for their quantification in pharmaceutical formulations.

Various parameters affecting the fluorescence intensity, i.e., sodium dodecyl sulfate (SDS) concentration, pH, volume fraction of solvents were optimized using RSM. Then, the optimized parameters were applied to the validation of a method for fluorimetric determination of β-blockers in their pharmaceutical preparations.

It is obtained that under the optimum conditions for determination of ATE, the method provided a linear range between 130 to 750 ng/mL with a coefficient of correlation (r) of 0.9996. Also, the limit of detection and limit of quantification (LOD and LOQ) were 40 ng/mL and 130 ng/mL, respectively. Moreover, it is observed that, the linearity of method for determination of CAR was between 0.37 to 4.0 ng/mL and LOD and LOQ of method were 0.11 ng/mL and 0.37 ng/mL, respectively.

An accurate, sensitive and reliable spectrofluorimetric method was developed anf successfully used to determine the (ATE) and carvedilol (CAR) in their pharmaceutical preparations.

Breast cancer is the most common cancer among the female population and its prevalence is increasing worldwide. Trastuzumab (Herceptin) therapy improves prognosis in HER2 positive patients, but Heart Failure (HF) is one of its known complication. In this study we aimed to assess potential benefits of prophylactic carvedilol therapy in patients receiving Herceptin.

65 HER2 positive breast cancer patients were enrolled in the study.  All of the patients received Herceptin. 27 patients also received carvedilol 6.25 mg twice daily and 38 patients had usual care. Echocardiography was performed at baseline and after 3 months in both groups and changes in cardiac function parameters were compared between two groups.

After 3 months, LA volume index (p value = 0.012), TAPSE (p value = 0.009), Tei index (p value = 0.015) and Lateral Longitudinal Strain (p value = 0.024) were significantly better in patients receiving carvedilol.

Carvedilol can be effective in prevention of systolic and diastolic dysfunction following Herceptin therapy.

This study was carried out to boost the pharmacologic influence of carvedilol (CAR) (as a poorly water-soluble drug) by developing CAR-eudragit® RS100 (Eud) nanofibers and nanobeads benefiting an electrospraying approach. CAR-Eud nanoformulations with varying ratios (1:5 and 1:10) at total solution concentrations of 10 %, 15 % and 20 % w/v were formulated. The solution concentration remarkably impressed the size and morphology of the samples; in which, the nanobeads (mean diameter of 135.83 nm) were formed at low solution concentrations and high concentrations led to nanofibers (mean diameter of 193.45 nm) formation. DSC thermographs and PXRD patterns along with FTIR spectrum precisely showed CAR amorphization and no probable chemical interactions between CAR and Eud in the electrosprayed nanosystems. The in vitro release considerations demonstrated that the nanoformulations with the drug: polymer ratios of 1:10 and 1:5 depict rapid dissolution rate compared to the physical mixtures (PMs) and the pure drug. The in vivo studies in Wistar male rats suggested that the electrosprayed nanoformulation (1:10; 20 %) reduced the isoproterenol (ISO) induced elevation of heart rate, necrosis and accumulation of neutrophils in the heart tissue more efficient than the pure drug and PM. Our finding illustrated that the electrospraying as a profitable one-step procedure could be productively benefited to improve the physicochemical features and pharmacologic influences of CAR.

Carvedilol (CVD) is an antihypertensive agent with a short half-life, pH-dependent solubility, and narrow absorption window. The purpose of this research was to prepare a floating-drug delivery-system of carvedilol to increase its half-life. The present study investigates the preparation of carvedilol-floating microspheres, evaluates the floating-drug delivery-system (FDDS) (by scanning electron microscope), it’s in vitro stability, and in vivo profile. Floating microspheres were prepared by solvent-evaporation (oil-in-water emulsion) technique using hydroxypropyl methylcellulose (HPMC) and ethyl cellulose (EC) as the rate controlling polymers. The surface morphology of the prepared microspheres w:as char:acterized by scanning electron microscopy. In this study, the particle size analysis, drug entrapment efficiency, surface morphology, buoyancy percentage, and release studies were performed. The microspheres were found to be spherical and porous. The results showed that the mean/mean (SD) values of tapped density, Carr's compressibility index, angle of repose, percentage yield, in vitro buoyancy, %entrapment efficiency of CVD-loaded floating microspheres were 0.42 (0.012), 12.5 (1.895), 23.5 (1.856), 80.2 %, 79.0 %, and 85.81(1.40), respectively. The developed floating-microsphere of CVD released the drug for 24 h and based on in vivo studies, the drug-loaded floating microspheres help in maintaining the mean (SD) systolic blood pressure within the range of 120 (0.32) to 120 (1.02) mmHg and diastolic pressure within 91 (0.71) to 92 (0.79) mmHg. Thus, floating microsphere of CVD offers a suitable and practical approach for prolonged release of the drug over an extended period, and thus improves the oral bioavailability and efficacy of the drug as well as the patient’s compliance.

Carvedilol, a non-specific β-blocker, has been used for treatment of hypertension, stroke and congestive heart failure. The therapeutic effects of β blockers in cancer patients have been shown. Carvedilol has considerable anti-inflammatory, anti-tumor and anti-angiogenic properties. In this study, the effects of carvedilol on proliferation of human U937 and Molt-4 leukemic cells were studied in vitro. Human leukemic T cells [Molt-4] and monocytes [U937] were cultured in Roswell Park Memorial Institute (RPMI) 1640 complete medium and were treated with different concentrations of carvedilol (1, 5, 10, 20, 50 and 100 μg/ml) for 24, 48 and 72 hours. The cytotoxicity of carvedilol on U937 and Molt-4 cells was determined using MTT (3-[4, 5 dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide) assay. Carvedilol significantly decreased human U937 and Molt-4 leukemic cells proliferation, concentration- and time-dependently in comparison with control cells. According to our results, carvedilol has anti-proliferative effect on U937 and Molt-4 leukemic cells in a concentration- and time-dependent manner. Thus, carvedilol might be a useful candidate for treatment of leukemic patients as well as other cancers.

Treatment-induced cardiotoxicity is one of the major side effects of trastuzumab treatment in patients with breast cancer. Left ventricular (LV) dysfunction is the leading cause of treatment-induced cardiotoxicity. The development of treatment-induced cardiotoxicity during cancer treatment may force patients to modify or quit the treatment. In this trial, we evaluated the prophylactic effects of carvedilol on LV dysfunction in patients with breast cancer receiving trastuzumab using 2D speckle-tracking echocardiography (2DSTE). We conducted an open-label randomized clinical trial and enrolled 71 non-metastatic HER-2 positive patients with breast cancer candidated to receive trastuzumab. Carvedilol was administered concomitantly with the trastuzumab standard regimen at a dosage of 6.25 mg twice a day and up-titrated to the maximum tolerated dosage. The 2DSTE parameters to evaluate the LV systolic and diastolic functions were evaluated initially and 3 months thereafter. Thirty-six patients were randomly assigned to the carvedilol group and 35 patients to the control group. The mean left ventricular ejection fraction (LVEF) was not significantly different either in both groups or between the 2 groups (P=.61) during the follow-up. In contrast, the global longitudinal strain of the LV (GLS) (P=.000) and the strain rate of the LV systolic function (SRS) (P=.004) as markers of the LV systolic function were reduced in the control group. Furthermore, the LV strain rate of the early (SRE) and late (SRA) diastolic functions were preserved in the patients who received prophylactic carvedilol (P=.000 and P=.005, respectively). Concomitant carvedilol treatment with a maximum tolerable dose in patients with non- metastatic HER2-positive breast cancer under treatment with trastuzumab might be effective on the reduction of systolic and diastolic echocardiographic findings other than the LVEF in patients with weak markers of heart failure.

A fast and simple method for extraction of carvedilol in human plasma samples based on salting out assisted liquid-liquid extraction (SALLE) is described. The method involving extraction of carvedilol with water-miscible organic solvent acetonitrile when solvent phase separation occurs using NaCl as a salt. The extracted phase was analyzed by high- performance liquid chromatography with ultra violet detection at 240 nm. The procedure has been optimized with respect to type and amount of salt, volume of sample, extraction solvent and the pH of solution. In the optimal condition the linear calibration range was 5-500 μg L-1 and the correlation coefficient was 0.9965. The limit of detection and limit of quantification were 1.0 µg L-1 and 3.3 μg L-1, respectively and a relative standard deviation of 3.5 % for five replicates were obtained. In spiking experiments on real samples, the average recoveries found by the present method were between 96.0% and 105.0%.

To investigate the cardioprotective potential of the aqueous extract of Allium cepa Linn. bulb in isoprenaline-induced myocardial injury in Wistar albino rats. In vitro total phenolic, total flavonoid content and 2, 2’-diphenyl-1-picrylhydrazyl hydrate radical scavenging activity was measured. Isoprenaline-induced myocardial injury model was used to evaluate in vivo effect of aqueous extract of A. cepa in Wistar albino rats. Seventy two rats were randomly divided in 6 groups. Rats were treated with A. cepa 400 mg/kg and 800 mg/kg doses for 30 days and myocardial injury was produced by subcutaneous injection of isoprenaline (ISO) 85 mg/kg on day 28 and 29. Carvedilol 1 mg/kg for 30 days served as active control. Electrocardiogram parameters, cardiac injury markers, oxidative stress markers and histopathological changes were evaluated in each group and compared using appropriate statistical tests. In vitro evaluation of aqueous extract of A. cepa showed significant antioxidant property. ISO produced significant myocardial injury as compared to normal control group (P 0.05). The aqueous extract of A. cepa 400 mg/kg was found to be cardioprotective against myocardial injury while A. cepa 800 mg/kg did not show significant cardioprotective activity. So, we presume that A. cepa might be effective within certain dose range only.

Niosomes are non‑ionic surfactant vesicles used as drug carriers for encapsulating both hydrophobic and hydrophilic drugs. The aim of this study is to evaluate the effect of different surfactants on the physical properties and stability of carvedilol niosomes designed to improve oral bioavailability.

Different niosomal formulations were prepared using a film hydration method, with various mixtures of different non‑ionic surfactants including Span 20, 40, and 60, and also Tween 20, 40, and 60, along with cholesterol. The physicochemical characteristics of the formulations were evaluated in vitro.

The drug encapsulation efficiency was reduced by using lauryl (C12) chain containing surfactants, that is, Span/Tween. Cholesterol content and drug entrapment were the main factors affecting the mean particle size of the niosomes. The drug release profiles from most of the formulations were fitted well with the Baker‑Lonsdale model, indicating a diffusion‑based drug release mechanism. Niosomes prepared from 50 and 40% of the cholesterol with 25 or 30% of Span/Tween 60 showed the highest stability due to their high transition temperature and solid state feature of these surfactants.

From the results obtained, it may be concluded that nanoniosomes are promising stable carriers for the oral delivery of carvedilol.

In the present study,cardioprotective effect of aqueous extract of Garcinia indica Linn. fruit rinds in isoprenaline-induced myocardial infarction in Wistar albino rats was evaluated. In vitro total phenolic, total flavonoid content and 2, 2’-diphenyl-1-picrylhydrazyl hydrate radical scavenging activity was measured. In vivo effect of aqueous extract of G. indica was evaluated in Wistar albino rats by isoprenaline-induced myocardial injury model. Thirty six rats were randomly divided in 6 groups. Rats were treated with G. indica 250 mg/kg and 500 mg/kg doses for 21 days and myocardial injury was produced by subcutaneous injection of isoprenaline 85 mg/kg on day 20 and 21. Carvedilol 1 mg/kg for 21 days served as active control. Electrocardiogram parameters, cardiac injury markers (serum troponin-I, uric acid, lactate dehydrogenase, creatinine kinase-MB, aspartate aminotransferase and alanine aminotransferase), oxidative stress markers (superoxide dismutase, catalase and malondialdehyde level) and histopathological changes were evaluated in each group and compared using appropriate statistical tests. In vitro evaluation of aqueous extract showed significant antioxidant property. Isoprenaline produced significant myocardial ischemia as compared to normal control group (P<0.05). Administration of G. indica in both the doses did not significantly recover the altered electrocardiogram, cardiac injury markers, oxidative stress markers and histopathological myocardial damage as compared to disease control group (P>0.05). The aqueous extract of G. indica was not found to be cardioprotective against myocardial injury. Further study with more sample size and higher dose range may be required to evaluate its cardioprotective effect.