Ischemic stroke causes brain damage and neuronal cell death by depriving oxygen and nutrients and releasing excessive levels of glutamate and intracellular calcium. Epigallocatechin gallate (EGCG) is a polyphenolic compound present in green tea. It has antioxidant, anti-inflammatory, and neuroprotective effects. Hippocalcin is a calcium binding protein that regulates calcium concentration, neuronal differentiation, neuronal excitability, and neuronal cell death. In this study, we investigated whether EGCG regulates the expression of hippocalcin in neurons and astrocytes after focal cerebral ischemia. Cerebral ischemia was induced by meddle cerebral artery occlusion (MCAO). EGCG (50 mg/kg) or PBS was injected into the abdominal cavity just before MCAO surgery. Neurobehavioral tests were performed to evaluate the effect of EGCG on neurological behavioral deficits 24 h after MCAO surgery. Immunofluorescence staining was performed to evaluate the positive response to hippocalcin in the cerebral cortex after MCAO surgery. We also detected the positive reactions of neuronal nuclear protein (NeuN) and glial fibrillary acidic protein (GFAP) as markers of neuron and astrocyte, respectively. MCAO caused severe neurological impairment and EGCG treatment attenuated these impairments. MCAO damage reduced the number of NeuN-positive cells and increased the number of GFAP-positive cells. This result indicates a decrease in neurons and an increase in astrocytes. However, EGCG alleviated these changes caused by MCAO damage. MCAO reduced the number of hippocalcin-positive cells in neurons and astrocytes, and EGCG treatment attenuated these reductions. Hippocalcin exerts neuroprotective effect through regulating intracellular calcium concentration. In conclusion, EGCG regulates the expression of hippocalcin in neurons and astrocytes and has neuroprotective effects in focal cerebral ischemia.

Baicalin is a flavonoid compound with many advantages, including anti-inflammatory agents and antioxidants. Lipopolysaccharide (LPS) is an endotoxin that induces neuronal damage through inflammatory response and oxidative stress reaction. This study was investigated the protective effects of baicalin on the oxidative stress and histopathological changes caused by LPS in hippocampus. Adult mice were divided into four groups; vehicle-treated, baicalin-treated, LPS-treated, and LPS and baicalin co-treated animals. Baicalin (10 mg/kg/day) and/or LPS (250 μg/kg/day) were intraperitoneally administered for seven consecutive days, and body weight was measured. Reactive oxygen species (ROS) level and lipid peroxidation level in the hippocampus were examined. Histopathological study was performed using hematoxylin and eosin staining manuals. LPS treatment decreased body weight and increased ROS and oxidative stress in the hippocampus. However, co-treatment with baicalin alleviated these changes caused by LPS. Severe histopathological changes were observed in the hippocampus of LPS-treated animals. Baicalin co-treatment attenuated the changes and preserved neuronal cells from LPS damage. These results showed that baicalin suppresses LPS-induced neuronal damage by alleviating oxidative stress in the hippocampus. Thus, this study demonstrated that baicalin exerts protective effects against LPS-induced oxidative stress in hippocampus.

Lipopolysaccharide (LPS)는 염증유발 cytokine 분비를 자극하고 염증을 유발하는 그람음성균의 내독소이다. 본 연구에서는 LPS가 신경아교세포 활성과 해마에 있는 nuclear factor kappa B (NF-κB) 매개 염증유발 요소를 조절하는지를 조사하였다. 성체 수컷 쥐를 대조군과 LPS를 투여한 실험군으로 무작위로 나누어 vehicle 또는 LPS (250 μg/kg)를 5일 동안 복강투여하고 무게를 측정했다. 해마의 활성산소와 과산화지방질 수준을 분석하고, 형태학적 연구를 위해 Hematoxylin and eosin 염색을 시행하였다. 또한, 해마에서 ionized calcium-binding adapter molecule 1 (Iba-1), glial fibrillary acidic protein (GFAP), NF-κB, interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α)의 발현을 확인하기 위해 Western blot 분석과 immunofluorescence 염색을 시행하였다. 그 결과, LPS를 투여한 쥐들의 체중이 감소하였다. LPS 투여는 활성산소와 과산화지방질 수준의 증가를 유발하였고 LPS를 투여한 쥐의 해마에서 심각한 조직병리학적 변화를 확인했다. 또한 LPS 투여는 신경교세포와 별아교세포의 표시물인 Iba-1과 GFAP의 발현을 증가시켰고, NF-κB의 발현과 IL-1β와 TNF-α와 같은 염증성인자의 발현을 증가시켰다. 이러한 결과들을 통해 LPS 투여는 해마손상과 염증반응을 유도한다는 것을 알 수 있고 LPS 투여가 해마조직에서 신경아교세포와 NF-κB에 매개된 염증인자들을 활성화시킨다는 것을 확인하였 다. 따라서, 본 연구는 LPS 투여는 해마조직에서 산화적 스트레스 증가와 염증인자 활성을 증가시켜 신경손상을 유도함을 보여준다.

In this paper, we present a finite-time sliding mode control (FSMC) with an integral finitetime sliding surface for applying the concept of graph theory to a distributed wheeled mobile robot (WMR) system. The kinematic and dynamic property of the WMR system are considered simultaneously to design a finite-time sliding mode controller. Next, consensus and formation control laws for distributed WMR systems are derived by using the graph theory. The kinematic and dynamic controllers are applied simultaneously to compensate the dynamic effect of the WMR system. Compared to the conventional sliding mode control (SMC), fast convergence is assured and the finite-time performance index is derived using extended Lyapunov function with adaptive law to describe the uncertainty. Numerical simulation results of formation control for WMR systems shows the efficacy of the proposed controller.