Promises of phytochemical based nano drug delivery systems in the management of cancer.

Cancer is the leading cause of human disease and death worldwide, accounting for 7.6 million deaths per year and projected to reach 13.1 million by 2030. Many phytochemicals included in traditional medicine have been utilized in the management of cancer. Conventional chemotherapy is generally known to be the most effective treatment of metastatic cancer but these cancerous cells might grow resistant to numerous anticancer drugs over time that resulting in treatment failure. This review tried to portray the advancement in the anticancer and chemopreventive effects of several phytochemicals and some of its members encapsulated in the nano-based delivery system of the drug. It comprises the issue associated with limited use of each phytoconstituents in human cancer treatment are discussed, and the benefits of entrapment into nanocarriers are evaluated in terms of drug loading efficiency, nanocarrier size, release profile of the drug, and in vitro and/or in vivo research and treatment testing, such as cytotoxicity assays and cell inhibition/viability.

A review on epidermal growth factor receptor's role in breast and non-small cell lung cancer.

Epithelial growth factor receptor (EGFR) is a cell surface transmembrane receptor that mediates the tyrosine signaling pathway to carry the extracellular messages inside the cell and thereby alter the function of nucleus. This leads to the generation of various protein products to up or downregulate the cellular function. It is encoded by cell erythroblastosis virus oncogene B1, so called C-erb B1/ERBB2/HER-2 gene that acts as a proto-oncogene. It belongs to the HER-2 receptor-family in breast cancer and responds best with anti-Herceptin therapy (anti-tyrosine kinase monoclonal antibody). HER-2 positive breast cancer patient exhibits worse prognosis without Herceptin therapy. Similar incidence and prognosis are reported in other epithelial neoplasms like EGFR + lung non-small cell carcinoma and glioblastoma (grade IV brain glial tumor). Present study highlights the role and connectivity of EGF with various cancers via signaling pathways, cell surface receptors mechanism, macromolecules, mitochondrial genes and neoplasm. Present study describes the EGFR associated gene expression profiling (in breast cancer and NSCLC), relation between mitrochondrial genes and carcinoma, and several in vitro and in vivo models to screen the synergistic effect of various combination treatments. According to this study, although clinical studies including targeted treatments, immunotherapies, radiotherapy, TKi-EGFR combined targeted therapy have been carried out to investigate the synergism of combination therapy; however still there is a gap to apply the scenarios of experimental and clinical studies for further developments. This review will give an idea about the transition from experimental to most advanced clinical studies with different combination drug strategies to treat cancer.

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.

Cardioprotective effect of 6-shogaol against hyperglycemia-induced toxicity in H9c2 cardiomyocytes via suppressing of NF-κB pathway.

Diabetic cardiomyopathy (DC) is a serious complication of diabetes. Apoptosis, inflammatory and ROS production are among the factors that are involved in the progression of diabetic cardiomyopathy. 6-shogaol is reported to inhibit apoptosis and reduce inflammatory and ROS production. This study aimed to study the effect of 6-shogaol (6S) on the progression of diabetic cardiomyopathy in vitro. To develop DC model, H9c2 cell line was exposed to high glucose (HG) level (33 M glucose) for 24 h and used as a model for diabetic cardiomyopathy. Another set of H9c2 cell lines were 1 h pretreated with different conc. of 6-shogaol (5-20 µM). Cell viability, apoptosis, ROS production, IL-6, TNF-alpha and NF-κB were estimated in these cell lines treated with HG level or pretreated with 6-shgoal before HG. Exposing cardiomyocytes H9c2 cells to HG produced dramatic changes in cell biology and chemistry. There is a significant reduction in cell viability and enhancement in cell apoptosis as compared with control. In addition, ROS production, IL-6, TNF-α levels were increased in H9c2 line treated with HG. Also, there is overexpression of NF-κB in cells treated with HG levels alone. On the other hand, pretreatment of cardiomyocytes H9c2 cells with 6-shogaol (5-20µM) significantly improved cell viability and reduced apoptosis, in addition, 6S at a dose of 10 µM abrogated the deleterious effects of HG on oxidative stress and inflammatory parameters via modulation of NF-κB pathway. Therefore, 6S has a potential protective effect against hyperglycemia-induced DC in vitro.