Biophoton imaging identification of delayed functional neural circuit injury after cerebral ischemia-reperfusion.

BACKGROUND: The evaluation of structural changes after stroke has made great progress; however, it remains difficult to evaluate functional neural changes. NEW METHOD: Here, we report a novel imaging technique that could monitor delayed functional neural circuit injury in an animal model of cerebral ischemia-reperfusion. The changes in 50 mM glutamate-induced biophotonic activities in functional neural circuits in rat brain slices after middle cerebral artery occlusion were investigated with an ultraweak biophoton imaging system. RESULTS: Six hours after ischemia-reperfusion, the rats presented a significant decrease in motion ability together with a large part of the unstained 2,3,5-Triphenyltetrazolium chloride (TTC) area in the ischemia-reperfusion side, whereas the intensity of the biophoton emissions was consistent on both the ischemia-reperfusion and non-ischemic sides of brain slices. Twenty-four hours after reperfusion, the behavior evaluation and TTC staining recovered slightly, and the intensity of the biophoton emissions was weaker on the ischemia-reperfusion side than on the contralateral side. One week after reperfusion, the behavioral test and TTC staining recovered to normal levels; however, the intensity of the biophoton emissions was decreased significantly on both the ischemia-reperfusion and contralateral sides, and such changes were even distinguished in different brain areas, such as the sensory and motor coteries and striatum. CONCLUSION: These findings suggest that delayed functional neural circuit injury induced by cerebral ischemia-reperfusion could be identified with biophoton imaging techniques, providing a novel functional evaluation method for animal models of cerebral ischemia-reperfusion.

Quantum energy levels of glutamate modulate neural biophotonic signals.

Glutamate is the most abundant excitatory neurotransmitter in the brain, and it plays an essential and important role in neural functions. Current studies have shown that glutamate can induce neural biophotonic activity and transmission, which may involve the mechanism of photon quantum brain; however, it is unclear whether such a mechanism follows the principle of quantum mechanics. Here we show that the action of glutamate on its receptors leads to a decrease in its quantum energy levels, and glutamate then partially or completely loses its function to further induce the biophotonic activity in mouse brain slices. The reduced quantum energy levels of glutamate can be restored by direct-current electrical discharges and the use of energy transfer of chloroplast photosynthesis; hence, the quantum energy recovered glutamate can again induce significant biophotonic activity. Furthermore, the changes in quantum energy levels of glutamate are related to the exchange and transfer of electron energy on its active hydrogen atom. These findings suggest that the glutamate-induced neural biophotonic signals may be involved in the transfer of the quantum energy levels of glutamate, which implies a quantum mechanism of neurotransmitter action.

Glycyrrhizin Protects Mice Against Experimental Autoimmune Encephalomyelitis by Inhibiting High-Mobility Group Box 1 (HMGB1) Expression and Neuronal HMGB1 Release.

The inflammatory mediator high-mobility group box 1 (HMGB1) plays a critical role in the pathogenesis of human multiple sclerosis (MS) and mouse experimental autoimmune encephalomyelitis (EAE). Glycyrrhizin (GL), a glycoconjugated triterpene extracted from licorice root, has the ability to inhibit the functions of HMGB1; however, GL's function against EAE has not been thoroughly characterized to date. To determine the benefit of GL as a modulator of neuroinflammation, we used an in vivo study to examine GL's effect on EAE along with primary cultured cortical neurons to study the GL effect on HMGB1 release. Treatment of EAE mice with GL from onset to the peak stage of disease resulted in marked attenuation of EAE severity, reduced inflammatory cell infiltration and demyelination, decreased tumor necrosis factor-alpha (TNF-α), IFN-γ, IL-17A, IL-6, and transforming growth factor-beta 1, and increased IL-4 both in serum and spinal cord homogenate. Moreover, HMGB1 levels in different body fluids were reduced, accompanied by a decrease in neuronal damage, activated astrocytes and microglia, as well as HMGB1-positive astrocytes and microglia. GL significantly reversed HMGB1 release into the medium induced by TNF-α stimulation in primary cultured cortical neurons. Taken together, the results indicate that GL has a strong neuroprotective effect on EAE mice by reducing HMGB1 expression and release and thus can be used to treat central nervous system inflammatory diseases, such as MS.