Flaxseed lignans alleviates isoproterenol-induced cardiac hypertrophy by regulating myocardial remodeling and oxidative stress.

Cardiovascular diseases, the leading global cause of death, are usually associated with cardiac hypertrophy (CH). CH is an adaptive response of the heart against cardiac overloading, but continuous CH accelerates cardiac remodeling and results in heart failure. Available CH therapies delay the progress of heart failure, but they often fail to control symptoms or restore quality of life. Although flaxseed lignans have been shown to have significant anti-oxidant, anti-hypertensive, anti-inflammatory, and anti-fibrotic effects in various cardiovascular diseases, little is known about their effect on CH. Thus, this study evaluated the therapeutic effect of flaxseed lignans on CH, which was induced by subcutaneous injections with isoproterenol (5 mg/kg b.w) for 14 consecutive days. Flaxseed lignans (200 mg/kg) was given orally for 4 weeks. Cardiac pathological remodeling was evaluated by echocardiography, after which morphometric, biochemical, histological, and ultrastructural analyses were performed. Flaxseed lignans significantly ameliorated CH structural and functional alterations as shown by echocardiography. Lignans also reduced the relative heart weight, significantly decreased the elevated CK-MB and the lipid peroxidation marker malondialdehyde, augmented the myocardial total antioxidant capacity, and ameliorated the histopathological and ultrastructural changes in cardiac tissues and prevented interstitial collagen deposition. The results demonstrate promising anti-hypertrophic effect of flaxseed lignans against isoproterenol-induced cardiac hypertrophy, via regulating myocardial remodeling and oxidative stress. Therefore, lignans could be used as potential pharmacological intervention in the management of CH.

Calanus oil attenuates isoproterenol-induced cardiac hypertrophy by regulating myocardial remodeling and oxidative stress.

Calanus oil, an oil extracted from the marine crustacean Calanus finmarchicus, is one of the richest sources of omega-3 and poly-unsaturated fatty acids. Although calanus oil has been shown to have a significant anti-hypertensive, anti-inflammatory, anti-fibrotic and anti-obesity effects in various cardiovascular diseases, but little is known about its effect on pathological cardiac hypertrophy. Thus, the present study was carried out to evaluate the therapeutic effect of calanus oil on cardiac hypertrophy. Cardiac hypertrophy was induced by subcutaneous injections with isoproterenol (5 mg/kg b.w) for 14 consecutive days. Calanus oil (400 mg/kg) was given orally for 4 weeks. Cardiac pathological remodeling was evaluated by echocardiography, after which morphometric, biochemical, histological and ultrastructural analyses were performed. Calanus oil treatment significantly ameliorated isoproterenol-induced structural and functional alterations in echocardiography. Calanus oil also reduced the relative heart weight, significantly decreased the elevated cardiac enzymes (LDH and CK-MB) and the lipid peroxidation marker (MDA), augmented the myocardial antioxidant status (TAC), and ameliorated the histopathological and ultrastructural changes in cardiac tissues and prevented interstitial collagen deposition. The present study, for the first time, provided morphometric, biochemical, histological and ultrastructural evidences supporting the promising anti-hypertrophic effect of calanus oil against ISO-induced cardiac hypertrophy. This anti-hypertrophic effect of calanus oil is via regulating myocardial remodeling and oxidative stress. Therefore, it could be used as potential pharmacological intervention in the management of cardiac hypertrophy.

Effect of dehydroepiandrosterone on the liver of perimenopausal rat: multiple doses study.

Dehydroepiandrosterone (DHEA) is a widespread nutritional "anti-aging" supplement. Exogenous supplementation of DHEA is now being commonly used to augment ovarian stimulation in perimenopausal women with diminished ovarian reserve. Whether DHEA causes side effects in such age is, however, unknown. Thus, this study investigates the effects of pharmacological doses of DHEA supplementation on the liver of perimenopausal rats. DHEA supplementation to perimenopausal rats resulted in slight hepatomegaly and steatosis, hepatocytic hypertrophy, mitochondrial swelling, elevation in serum alanine aminotransaminase levels, in addition to the accumulation of lipid droplets and lipolysosomes in a dose-dependent manner. In conclusion, long-term administration of high doses of DHEA causes ultrastructural alterations and changes in the levels of cholesterol and triglyceride in hepatocytes of perimenopausal rats. DHEA at a dose of 50 mg/kg improves health and decreases the body weight, with the least side effects on the liver of perimenopausal rats.

Morin attenuates sepsis-induced acute kidney injury by regulating inflammatory responses, oxidative stress and tubular regeneration (morin and sepsis-induced acute kidney injury).

Sepsis-associated acute kidney injury (AKI) is a health complication, encompassing excessive inflammatory response, oxidative stress, and tubular necrosis; leading to kidney failure and death. Sepsis treatments are nonspecific and palliative. In this study, we evaluated the effect of morin, a flavonoid with known nephroprotective capabilities, on sepsis-induced AKI by dividing eighty male mice into: normal, morin-treated, septic, and septic mice treated with morin. Half of the groups were sacrified 3 days post sepsis induction, while the rest was sacrified on the 7th day. Treating septic mice with morin resulted in the amelioration of sepsis-associated pathophysiological renal alterations and the increase of the survival and recovery rates compared with those of septic control group. These findings indicate that morin has a therapeutic effect against sepsis-associated AKI via its anti-inflammatory, antioxidant and regenerative effects. Thus, it could be used as potential pharmacological intervention for preventing renal complications of sepsis.

Spirulina inhibits hepatocellular carcinoma through activating p53 and apoptosis and suppressing oxidative stress and angiogenesis.

BACKGROUND: Most hepatocellular carcinoma cases are diagnosed at late stages of the disease, which makes it the second cause of cancer mortality worldwide. For advanced-stage patients, chemotherapeutic drugs are the best treatment option; however, their adverse effects and high cost are still major obstacles for effective treatment. Spirulina microalga is a rich source of nutritional and bioactive elements and potential pharmaceuticals, which has an -proliferative effect against several cancer cell lines. It also has a prophylactic effect against the early stages of some cancer models, including hepatocellular carcinoma. AIMS: The present study was carried out to evaluate the therapeutic anticarcinogenic effect of spirulina against advanced murine hepatocellular carcinoma. MAIN METHODS: Hepatocarcinoma was induced by a single injection of diethylnitrosamine (100 mg/kg, intraperitoneally) followed by 22 weekly injections of carbon-tetrachloride (0.5 mg/kg, i.p). Spirulina (250 and 500 mg/kg bw) was given orally, from week 25 to 28, after the establishment of hepatocellular carcinoma. KEY FINDINGS: Spirulina inhibited HCC structural and functional alterations, manifested by improving the survival rate, significantly decreasing the tumor marker AFP, and the count and size of the hepatic nodules, as well as downstaging HCC. This was accompanied with the augmentation of the endogenous antioxidant capacity, apoptosis (Bax) and the tumor suppressor protein (p53), as well as the suppression of tissue levels of the lipid peroxidation marker (MDA) and neoangiogenesis marker (VEGF). SIGNIFICANCE: In conclusion, spirulina has an anticarcinogenic effect against advanced hepatocellular carcinoma exerted through activating the tumor suppressor protein p53 and apoptosis, and suppressing oxidative stress and angiogenesis.

Effects of dehydroepiandrosterone on the ovarian reserve and pregnancy outcomes in perimenopausal rats (DHEA and fertility in perimenopausal rats).

BACKGROUND: Dehydroepiandrosterone (DHEA) is a weak androgen and a crucial precursor of sex steroids. Exogenous supplementation of DHEA is now being commonly used to augment ovarian stimulation in women with diminished ovarian reserve. However, the effects of DHEA are controversial. AIMS: This study verifies the effects of pharmacologic doses of DHEA on the ovarian reserve variables, follicular development, reproductive function, and pregnancy outcomes of perimenopausal rats. MAIN METHODS: The reproductive function was studied by monitoring the estrous cycle and hormones. The ovarian reserve was studied by testing the anti-mullerian hormone and ovarian histology. The follicular development was studied histologically and immunohistochemically. KEY FINDINGS: DHEA supplementation at a dose of at 50 mg/kg improved the ovarian reserve and pregnancy outcomes. Higher doses of DHEA caused PCOs-like symptoms manifested by the development of cystic follicles and low ovarian reserve and pregnancy outcomes. SIGNIFICANCE: DHEA is a promising treatment that improves the ovarian reserve parameters and pregnancy outcomes. Further studies are needed to determine the optimal dose and duration.