[Effects of the rice straw on Microcystis aeraginosa analyzed by different physiological parameters].

The growth and physiology of bloom-forming cyanobacterium Microcystis aeruginosa were determined by the flow cytometry when exposed to rice straw extract for 15 d. The cell growth, cell integrity, mitochondrial transmembrane potential, and esterase activity were used to evaluate the physiological response in Microcystis aeruginosa. Rice straw extract stored for 5 days significantly inhibited the growth of Microcystis aeruginosa in a concentration-dependent way; Most of the algae cells (> 98%) remained complete membranes in all the concentration treatments; Compared with the control cultures, the rice straw induced both negative and positive effects on the esterase activity for each test within 4 days, while the inhibition exceeded the stimulation effect. After a 7 d exposure, only the inhibition effect was found. Neither the inhibited nor stimulated effects was observed after algae exposure from 10 d to 15 d. Evident changes was found in the membrane potential during 7 d experiment, whereas inhibition effect became weaker after 10 d and 15 d exposure, in consistent with the result of esterase activity. These results confirmed that the rice straw extract might provide both dominant inhibition and relatively weak stimulation effects. After a long time exposure, inhibition effect became limited while stimulation effect disappeared. The action of rice straw may be algistatic (preventing algal growth) but not algicidal (killing algae).

Stabilization of mitochondrial function by tetramethylpyrazine protects against kainate-induced oxidative lesions in the rat hippocampus.

Mitochondria are critical regulators of cell death, a key feature of neurodegeneration. Reactive oxygen species (ROS) are crucial to Ca(2+)-mediated effects of glutamate receptor activation leading to neuronal degeneration. Tetramethylpyrazine (TMP) is a principal ingredient of Ligusticum wallichi Franchat (a Chinese herb), used for treatment of cardiovascular and cerebrovascular ischemic diseases. However, its protection against oxidative brain injury associated with excessive activation of glutamate receptors is unknown. In this study, we demonstrate TMP neuroprotection against kainate-induced excitotoxicity in vitro and in vivo. We found that TMP could partly alleviate kainate-induced status epilepticus in rats and prevented and rescued neuronal loss in the hippocampal CA3 but not the CA1 region. The partial prevention and rescue of neuronal loss by TMP were attributable to the preservation of the structural and functional integrity of mitochondria, evidenced by maintaining the mitochondrial membrane potential, ATP production, and complex I and III activities. Stabilization of mitochondrial function was linked to the observation that TMP could function as a reductant/antioxidant to quench ROS, block lipid peroxidation, and protect enzymatic antioxidants such as glutathione peroxidase and glutathione reductase. These results suggest that TMP may protect against oxidative brain injury by stabilization of mitochondrial function through quenching of ROS.