With our DCFDA observations pertaining to the effects of CP on the oxalate treated cells, here also it could be appreciated that there is a measurable restoration of the GDC-0199 abmole bioscience mitochondrial potential due to CP, lending credence to our earlier observations. Reports suggest the involvement of JNK in apoptotic signals. It has also been shown that extracellular stress-related kinase activation inhibits apoptosis, whereas cytokine induced apoptosis is mediated by JNK. In our in vitro study, the disappearance of JC-1 staining AB1010 indicated mitochondrial collapse through depolarization of the mitochondrial membrane. We hypothesize that oxalate induced mitochondrial injury preceded a change in gene expression in the renal tubular cells. Decreased ATP levels, increased ROS and HEL levels indicated an increase in oxidative stress in renal tubular cells. Increased stress induced kinases JNK and ERK1/2 expression, decreased ATP levels and decreased cell viability were indicative of mitochondrial collapse and loss of mitochondrial membrane potential through induction of the apoptotic pathway by oxalate injury. In a nutshell, one can therefore construe about essentially two broad concepts, namely oxalate-induced oxidative stress and CP induced anti-oxidative response, which can be a part of the overarching hypothesis that tries to explain the pathogenic mechanisms of oxalate-induced nephrotoxicity and the role of antioxidant defense measures in countering the detrimental consequences of oxalate. Our present study is one of the first steps to show that oxalate induces increased ROS production, which might themselves mediate mitochondrial membrane permeability transition culminating in a leaky mitochondrion. Our study throws light on the sites where CP might be active in that, the endogenous pool of cellular antioxidants goes up and at a molecular level, the levels of mitochondrial membrane potential and ATP production are enhanced and cell stress is aborted by CP. Further studies to strengthen our current observations that CP could significantly prevent oxalate-mediated LPO and cellular stress-induced MAP kinases may be warranted. Therefore, our current investigation marks the beginning of an exciting novel therapeutic strategy against oxidative stress-associated diseases. Studies on brain connectivity have advanced considerably and helped to understand cognition efficiency and relevant impairment in neurobiological diseases. Numerous functional connectivity studies have found that the brain has both high local clustering coefficiency and optimal global integration, similar to a smallworld network. Only a few studies have explored the relationships of structural connectivity and functional activity. A developmental study found that white matter connectivity supports brain-wide coherence and synchrony. Another study showed decoupling between functional and structural connectivity in Schizophrenia patients. These studies indicated that combining functional and structural neuroimaging studies can more comprehensively assess the altered brain connectivity in different clinical conditions. Parallel with the division of clustering and global integration in functional connectivity study, the structural connectivity can further be divided into regional short-range fibers that specified for local connectivity and long-range fiber for more global connectivity.