Anti-asthmatic and antioxidant activity of flavonoids isolated from Mentha longifolia subspecies typhoides (Briq.) Harley. and Mentha longifolia subspecies schimperi (Briq.) Briq. on ovalbumin-induced allergic asthma in mice: In-vivo and in-silico study.

Ethnopharmacological Relevance: Mentha longifolia L. has been employed to treat cough, lung inflammation, and bronchial asthma disorders.

Aim Of The Study: Our study was carried out to investigate the medicinal effect of the flavonoids derived from M.

Effect of sacubitril/valsartan on cognitive impairment in colchicine-induced Alzheimer's model in rats.

Alzheimer's disease (AD) is a complex neurodegenerative disease. There is epidemiological evidence that heart failure (HF) patients are at higher risk of developing AD, and the impact of sacubitril/valsartan, the first angiotensin receptor-neprilysin inhibitor (ARNI) approved for HF, on cognitive functions is still controversial. To investigate the effect of sacubitril/valsartan on cognitive functions in colchicine-induced AD rat model.

Study of cardioprotective activity of the methanolic extract of the aerial parts of compared to against adrenaline-induced myocardial toxicity in rats.

Cardiovascular ailments result in a great rate of mortality all over the world. Myocardial infarction is a common presentation of cardiovascular disease. The current work aimed to investigate and compare the cardioprotective potentials of methanolic extracts from the aerial parts from and in adrenaline-induced cardiotoxicity in rats.

Sildenafil citrate increases myocardial cGMP content in rat heart, decreases its hypertrophic response to isoproterenol and decreases myocardial leak of creatine kinase and troponin T.

Background: Cardiac hypertrophy is a major risk factor for morbidity and mortality in a number of cardiovascular diseases. Consequently, the signaling pathways that inhibit cardiac hypertrophy are currently receiving much interest. Among them, nitric oxide (NO), signaling via cGMP and cGMP-dependent protein kinase I, has been recognized as a negative regulator of cardiac hypertrophy.