From the structural point of view, it is evident that mangiferin contains four polyphenolic H-atoms. Two of them could easily be abstracted by suitable free radicals to form two stable phenoxyl radicals and this property of mangiferin probably explain its free radical scavenging activity. In conclusion, results from our study revealed that Pb not only activates NF-kB activation via IKK pathway in the liver tissue but also remains responsible for the increased phosphorylation of MAPKs and ultimately leads to hepatic cellular apoptosis via mitochondria dependent pathway. Mangiferin, on the other hand, could act as a protective agent in this Pb induced pathophysiology by enhancing antioxidant defense and acting through the mitochondrial dependent as well as via the inhibition of MAPKs and NF-kB pathways. In other words, mangiferin supplementation appears to be a promising approach for the hepatoprotection in Pb-induced liver dysfunction and cell death. This xanthone, therefore, deserves further research as a potent beneficial agent in hepatic and other organ pathophysiology because of the absence of any noticeable toxicity and its multiple advantageous properties. Non-small cell lung cancer is the most common cause of cancer-related deaths worldwide. The average 5-year survival rate is less than 15%, which has remained largely unchanged for the last three decades. The majority of NSCLC patients present with advanced disease at diagnosis, and those diagnosed with early stage disease often experience recurrence and metastatic disease. Host immune cells mediate immune surveillance by eradicating aberrant cells, and this is compromised in a tumor-promoting microenvironment for many patients with lung cancer. Several immune defects, including a shift toward the type 2 helper T cell phenotype, are evident in lung cancer patients. However, the same immune cells may promote tumor growth and metastasis through angiogenesis and invasion of the extracellular matrix. Understanding the fundamental molecular processes that cause these defects would provide an opportunity to develop innovative therapies. In addition, immune cell responses mounted by various histopathological types and tumor stages of lung cancer may be different; however, studies on this issue are lacking. Several immunosuppressive molecules are produced by tumors, such as interleukin-10, transforming growth factor-beta, or Masitinib cyclooxygenase-2 metabolites; however, specific therapies such as Temozolomide chemotherapy and radiotherapy may contribute to the alteration of immune system function. Increasing evidence suggests that a facet of immune surveillance can be restored by appropriate chemotherapy agents. For example, the nucleoside analogue gemcitabine has been shown to selectively enhance the adaptive immune response and promote the cell-mediated immune response over the humoral immune response in addition to conventional apoptotic effects. In addition, the platinum-based agent, cisplatin, has been shown to augment the anti-tumor effects of cytotoxic Tlymphocyte-mediated immunotherapy. It has also been demonstrated that using platinum-based double chemotherapy yields a significant benefit in terms of tumor response and survival compared with a single-agent regimen. The underlying mechanism of immune potentiation for combination chemotherapy is largely unknown. The aim of this study was to improve the understanding of the molecular mechanisms that regulate.