Time representation of mitochondrial morphology and function after acute spinal cord injury

Changes in mitochondrial morphology and function play an important role in secondary damage after acute spinal cord injury. We recorded the time representation of mitochondrial morphology and function in rats with acute spinal cord injury. Results showed that mitochondria had an irregular shape, and increased in size. Mitochondrial cristae were disordered and mitochondrial membrane rupture was visible at 2–24 hours after injury. Fusion protein mitofusin 1 expression gradually increased, peaked at 8 hours after injury, and then decreased to its lowest level at 24 hours. Expression of dynamin-related protein 1, amitochondrial fission protein, showed the opposite kinetics. At 2–24 hours after acute spinal cord injury, malondialdehyde content, cytochrome c levels and caspase-3 expression were increased, but glutathione content, adenosine triphosphate content, Na＋-K＋-ATPase activity and mitochondrial membrane potential were gradually reduced. Furthermore, mitochondrial morphology altered during the acute stage of spinal cord injury. Fusion was important within the first 8 hours, but fission played a key role at 24 hours. Oxidative stress was inhibited, biological productivity was diminished, and mitochondrial membrane potential and permeability were reduced in the acute stage of injury. In summary, mitochondrial apoptosis is activated when the time of spinal cord injury is prolonged.

Stimulating mitochondria to protect the brain following traumatic brain injury

Traumatic brain injury （TBI） is an acquired injury to the brain that occurs with sudden trauma that can range from mild （concussive） to severe. TBI is considered a leading cause of death in children and young adults, with the Centers for Disease Control and Prevention estimating that approximately 1.7 million cases of TBI occur in the United States annually （Faul et al., 2010）. Further, since the begin- ning of the global war on terrorism, the Department of Defense has reported over 344,000 U.S. Service Members have been diagnosed with traumatic brain injury from penetrating injuries to mild forms of TBI. TBI, caused by a sudden impact, penetration, or rapid move- ment of the brain, interrupts the normal functioning of the brain. While the intracranial location and severity of injury contribute to the extent of functional deficits.

3′-Daidzein sulfonate sodium improves mitochondrial functions after cerebral ischemia/reperfusion injury

3′-Daidzein sulfonate sodium is a new synthetic water-soluble compound derived from daidzein（an active ingredient of the kudzu vine root）. It has been shown to have a protective effect on cerebral ischemia/reperfusion injury in rats. We plan to study the mechanism of its protective effect. 3′-Daidzein sulfonate sodium was injected in rats after cerebral ischemia/reperfusion injury. Results showed that 3′-daidzein sulfonate sodium significantly reduced mitochondrial swelling, significantly elevated the mitochondrial membrane potential, increased mitochondrial superoxide dismutase and glutathione peroxidase activities, and decreased mitochondrial malondialdehyde levels. 3′-Daidzein sulfonate sodium improved the structural integrity of the blood-brain barrier and reduced blood-brain barrier permeability. These findings confirmed that 3′-daidzein sulfonate sodium has a protective effect on mitochondrial functions after cerebral ischemia/reperfusion injury, improves brain energy metabolism, and provides protection against blood-brain barrier damage.

Underlying mechanism of protection from hypoxic injury seen with n-butanol extract of Potentilla anserine L. in hippocampal neurons

The alcohol and n-butanol extract of Potentilla anserine L. significantly protects myocardium from acute ischemic injury. However, its effects on rat hippocampal neurons and the mechanism of protection remain unclear. In this study, primary cultured hippocampal neurons from neonatal rats were incubated in 95% N2 and 5% CO2 for 4 hours. Results indicated that hypoxic injury decreased the viability of neurons, increased the expression levels of caspase-9 and caspase-3 mRNA, as well as cytochrome c, Caspase-9, and Caspase-3 protein. Pretreatment with 0.25, 0.062 5, 0.015 6 mg/mL n-butanol extract of Potentilla anserine L. led to a significant increase in cell viability. Expression levels of caspase-9 and caspase-3 mRNA, as well as cytochrome c, Caspase-9, and Caspase-3 protein, were attenuated. The neuroprotective effect of n-butanol extract of Potentilla anserine L. was equivalent to tanshinone IIA. Our data suggest that the n-butanol extract of Potentilla anserine L. could protect primary hippocampal neurons from hypoxic injury by deactivating mitochondrial cell death.

Case report of unilateral electric cataract with transmission electron microscopy image

Dear Sir,We hereby report a case of unilateral electric cataract with transmission electron microscopy（TEM）image.Ocular injuries induced by electricity can occur simultaneously or sequentially with the electric event,and occasionally occur later than the initial event.There are many ocular manifestations,with the most common one being

Protective effect of Shenfu injection on myocardial mitochondria injured by ischemia-reperfusion in rabbits

The main active components of Shenfu injection (SFI), an extract of traditional Chinese herbs, are ginsenoside and higenamine. Ginsenoside can improve ischemic myocardium metabolism, scavenge free radicals, protect myocardial ultrastructure and reduce Ca^(2+) overload. Higenamine can enhance heart contractility, improve coronary circulation and decrease the effect of acute myocardial ischemia. SFI was found to have had some cardiac protective effect during cardiopulmonary bypass.^(1,2) SFI was added into St. Thomas crystal cardioplegic solution in this study to investigate the protective effect of SFI on ischemic-reperfused rabbit heart and to observe the influence on mitochondrial oxygen free radical (OFR), Ca^(2+) and mitochondrial ultrastructure.