Role of Various Gene Expressions in Etiopathogenesis of Type 2 Diabetes Mellitus.

CONTEXT: Diabetes is a metabolic disease, with high mortality, and is characterized by increased glucose levels in the blood occurring due to poor pancreatic insulin secretion or development of insulin resistance in the body. Type 2 DM (T2DM) represents 90% of diabetic cases, and its pathogenesis involves a genetic correlation with insulin resistance, ß-cell dysfunction, lifestyle, and environmental factors. OBJECTIVE: The current study intended to examine the pathophysiology of T2DM, including factors influencing insulin resistance and beta (ß)-cell dysfunction as well as the genetic factors that indicate susceptibility to T2DM. DESIGN: The research team performed a narrative review by searching the Mendeley, Science Direct, Medline, PubMed, Google Scholar, and Springer databases. The search used the keywords Diabetes, insulin secretion and environmental factor. SETTING: This study was take place in School of Pharmacy, Suresh Gyan Vihar University, Jaipur, India. RESULTS: The paraoxonase-1 gene Q192R and the L55M, INS-VNTR, and IL-38 gene alterations can result in insulin resistance while PAM variants and miR-132 and miR-18 expression can lead to ß-cell dysfunction. Palmitate-like FFA expression of mRNA MafA, and IRS-2 can lead to impairment of insulin secretion. CONCLUSIONS: T2DM is the most common metabolic disorder of the twenty-first century, and its incidence, complications, and morbidity increase every day. The examination of T2DM's pathophysiology and the literature review have revealed that it has a strong correlation with genetic defects.

Role of Flavonoids in Management of Various Biological Targets in Alzheimer's Disease: Evidence from Preclinical to Clinical Studies.

More than 10 million people worldwide have Alzheimer's disease (AD), a degenerative neurological illness and the most prevalent form of dementia. AD's progression in memory loss, cognitive deterioration, and behavioral changes are all symptoms. Amyloid-beta 42 (Aß42), the hyperphosphorylated forms of microtubule-associated tau protein, and other cellular and systemic alterations are all factors that contribute to cognitive decline in AD. Rather than delivering a possible cure, present therapy strategies focus on reducing disease symptoms. It has long been suggested that various naturally occurring small molecules (plant extract products and microbiological isolates, for example) could be beneficial in preventing or treating disease. Small compounds, such as flavonoids, have attracted much interest recently due to their potential to alleviate cellular stress. Flavonoids have been proven helpful in various ways, including antioxidants, anti-inflammatory agents, and anti-apoptotic agents, but their mechanism remains unknown. The flavonoid therapy of Alzheimer's disease focuses on this review, which includes a comprehensive literature analysis.

An overview of epithelial growth factor receptor (EGFR) inhibitors in cancer therapy.

Epithelial growth factor receptor (EGFR), a transmembrane receptor on the cell surface, carries extracellular messages into the cell and alters the activity of the nucleus through tyrosine signalling. EGFR-targeted treatments have influenced the new era of precision oncology throughout the last few decades. Despite significant progress, long-term remission from solid tumours is still a distant goal for many oncologists. There are several methods by which tumour cells alter the activity of this protein in solid tumours. EGFR-related oncogenic pathways, resistance mechanisms, and novel avenues to suppress tumour development and metastatic spread were discovered in clinical specimens using preclinical models (cell cultures, xenografts, mouse models), which were then validated in those specimens. EGFR has been implicated in the onset and advancement of a variety of cancers, according to research. An overview of EGFR's structural anatomy and physiology, its role in cancers, and clinical studies that target EGFR in various tumours are included in this review.

Nuclear factor-kappa B (NF-κB) inhibition as a therapeutic target for plant nutraceuticals in mitigating inflammatory lung diseases.

Nutraceuticals are dietary supplements that are used to improve health, postpone aging, prevent illnesses, and maintain the human body's correct functioning. Nutraceuticals are now garnering a lot of interest because of their nutritional and therapeutic benefits. The research indicating the relevance of nutraceuticals as a possible therapeutic candidate against inflammatory lung disease was covered in this review. Nowadays, inflammatory lung diseases such as chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, asthma, pneumonia, lung cancer, becoming highly dreadful because of their associated fatality. Inflammation is one of the cores and common factors of these diseases which is mainly associated with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, NF-κB p65 and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) phosphorylation, and initiation of the signaling pathway of the NF-κB. The secondary metabolites from natural sources are the active component that attenuates NF-κB and the associated pathway that inhibits inflammation in lung diseases. Nutraceuticals belonging to the chemical category polyphenols, alkaloids, terpenoids, flavonoids, tannins have the potential to combat the NF-κB pathway. Accordingly, this review discusses the medical value of nutraceuticals briefly and their ability to mitigate various inflammatory lung diseases through targeting inhibition of NF-κB.

Nuclear factor-kappa B and its role in inflammatory lung disease.

Nuclear factor-kappa B, involved in inflammation, host immune response, cell adhesion, growth signals, cell proliferation, cell differentiation, and apoptosis defense, is a dimeric transcription factor. Inflammation is a key component of many common respiratory disorders, including asthma, chronic obstructive pulmonary disease (COPD), bronchiectasis, and acute respiratory distress syndrome. Many basic transcription factors are found in NF-κB signaling, which is a member of the Rel protein family. Five members of this family c-REL, NF-κB2 (p100/p52), RelA (p65), NF-κB1 (p105/p50), RelB, and RelA (p65) produce 5 transcriptionally active molecules. Proinflammatory cytokines, T lymphocyte, and B lymphocyte cell mitogens, lipopolysaccharides, bacteria, viral proteins, viruses, double-stranded RNA, oxidative stress, physical exertion, various chemotherapeutics are the stimulus responsible for NF-κB activation. NF-κB act as a principal component for several common respiratory illnesses, such as asthma, lung cancer, pulmonary fibrosis, COPD as well as infectious diseases like pneumonia, tuberculosis, COVID-19. Inflammatory lung disease, especially COVID-19, can make NF-κB a key target for drug production.