The Anti-Inflammatory Compound Curcumin Enhances Locomotor and Sensory Recovery after Spinal Cord Injury in Rats by Immunomodulation.

Well known for its anti-oxidative and anti-inflammation properties, curcumin is a polyphenol found in the rhizome of Curcuma longa. In this study, we evaluated the effects of curcumin on behavioral recovery, glial scar formation, tissue preservation, axonal sprouting, and inflammation after spinal cord injury (SCI) in male Wistar rats. The rats were randomized into two groups following a balloon compression injury at the level of T9-T10 of the spinal cord, namely vehicle- or curcumin-treated.

ATP-site binding inhibitor effectively targets mTORC1 and mTORC2 complexes in glioblastoma.

The PI3K-AKT-mTOR signaling axis is central to the transformed phenotype of glioblastoma (GBM) cells, due to frequent loss of tumor suppressor PTEN (phosphatase and tensin homolog deleted on chromosome 10). The mechanistic target of rapamycin (mTOR) kinase is present in two cellular multi-protein complexes, mTORC1 and mTORC2, which have distinct subunit composition, substrates and mechanisms of action. Targeting the mTOR protein is a promising strategy for GBM therapy.

Stem cell therapy and curcumin synergistically enhance recovery from spinal cord injury.

Acute traumatic spinal cord injury (SCI) is marked by the enhanced production of local cytokines and pro-inflammatory substances that induce gliosis and prevent reinnervation. The transplantation of stem cells is a promising treatment strategy for SCI. In order to facilitate functional recovery, we employed stem cell therapy alone or in combination with curcumin, a naturally-occurring anti-inflammatory component of turmeric (Curcuma longa), which potently inhibits NF-κB.

Deconstructing mTOR complexes in regulation of Glioblastoma Multiforme and its stem cells.

Atypical serine-threonine kinase, mTOR (mechanistic target of Rapamycin; originally coined "mammalian TOR"), exists in two distinct multi-protein complexes termed mTOR complex 1 (mTORC1) and 2 (mTORC2), that senses and integrates a variety of environmental signals to control organism growth and homeostasis via non-overlapping signaling pathways. mTOR belongs to the phosphoinositide 3-kinase (PI3-K)-related kinase family, and an aberrant activation of mTORC1 is a potential contributing factor in uncontrolled cell growth, proliferation, and survival of tumor cells via specific effects on cap-dependent translation initiation, as well as in a more sustained manner via advancing ribosome biogenesis. It is thereby shown to be deregulated in numerous pathological conditions including cancer, obesity, type 2 diabetes, and neurodegeneration.