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Chronic inflammation plays an imperative role in the onset and progression of chronic diseases including diabetes , hypertension, cancer, allergies, and asthma. Diet can modulate different stages of inflammation since it is a rich source of antioxidants and bioactive compounds. Flavonoids are bioactive compounds abundantly found in various food groups such as vegetables, fruits, nuts, cereals, and beverages. Recent work on flavonoids has unveiled their potential to regulate or inhibit inflammation. This is attributed to their anti-inflammatory, anti-oxidative, and immune-modulatory properties, making flavonoids an invaluable component in nutraceutical, pharmaceutical, and medicinal applications. However, information related to their anti-inflammatory mechanism is still not well understood. The current review is an attempt to elaborate chemical structure, dietary sources, and anti-inflammatory properties of flavonoids against allergic diseases.
Despite large investments by industry and governments, no disease-modifying medications for the treatment of patients with Alzheimer's disease (AD) have been found. The failures of various clinical trials indicate the need for a more in-depth understanding of the pathophysiology of AD and for innovative therapeutic strategies for its treatment. Here, we review the rational for targeting IP3 signaling, cytosolic calcium dysregulation, phosphodiesterases (PDEs), and secondary messengers like cGMP and cAMP, as well as their correlations with the pathophysiology of AD. Various drugs targeting these signaling cascades are still in pre-clinical and clinical trials which support the ideas presented in this article. Further, we describe different molecular mechanisms and medications currently being used in various pre-clinical and clinical trials involving IP3/Ca⁺² signaling. We also highlight various isoforms, as well as the functions and pharmacology of the PDEs broadly expressed in different parts of the brain and attempt to unravel the potential benefits of PDE inhibitors for use as novel medications to alleviate the pathogenesis of AD.
Visceral leishmaniasis, a parasitic infectious diseases, is amongst the six largest killer infections, worldwide. It is caused by the protozoan parasites of the genus Leishmania. Nowadays, many advance treatments, formulations, and new therapeutic events occur in the treatment of visceral leishmanias, but till date, control of VL primarily relies upon the chemotherapeutic options. The available treatment options for visceral leishmaniasis include pentavalent antimonials, amphotericin B (deoxycholate and liposomal), miltefosine, and paromomycin. Since 1970s, the pentavalent antimonial drug has been the first-line treatment for visceral leishmaniasis where resistance is not reported. However, only after 20 years, there is a huge increase in treatment failure due to resistance of antimonials against VL, which made it banned in endemic areas of India and Nepal. Alternatively, amphotericin B was introduced as a first-line treatment for VL with high efficacy, but its nephrotoxicity and slow intravenous formulation make a hurdle for its success. Since its liposomal formulations have shown good efficacy with less toxicity, it is therefore approved as a best chemotherapeutic option. The limitations of this drug are high cost and instability at high temperature. Miltefosine was introduced in 2000s as the first oral drug for the treatment of visceral leishmaniasis with great antileishmanial activity. However, occurrence of resistance against it makes a hurdle in the path of its efficacy. Paromomycin has also shown good efficacy, with minor toxicity by altering the membrane potential and lipid metabolism. Recent clinical studies show that new formulation of antileishmanial drugs against different targets presents new benefits in chemotherapy in India.
