Search

Central nervous system tumors are classified as diseases of special clinical significance with high disability and high mortality. In addition to cerebrovascular diseases and craniocerebral injuries, tumors are the most common diseases of the central nervous system. Hydrogen sulfide, the third endogenous gas signaling molecule discovered in humans besides nitric oxide and carbon monoxide, plays an important role in the pathophysiology of human diseases. It is reported that hydrogen sulfide not only exerts a wide range of biological effects, but also develops a certain relationship with tumor development and neovascularization. A variety of studies have shown that hydrogen sulfide acts as a vasodilator and angiogenetic factor to facilitate growth, proliferation, migration and invasion of cancer cells. In this review, the pathological mechanisms and the effect of hydrogen sulfide on the central nervous system tumors are introduced.

In this study, we aimed to evaluate the effect of Nobiletin (NOB) on the placenta of Sprague–Dawley (SD) rats that had undergone reduced uterine perfusion pressure (RUPP) surgery and to evaluate the safety of NOB intervention during pregnancy. The results showed that NOB alleviated placental hypoxia, attenuated placental cell apoptosis, and inhibited placental damage in RUPP rats. No side effect of NOB intervention during pregnancy was observed. BeWo cell lines with P53 knockdown were then constructed using lentiviral transfection, and the P53 signaling pathway was found to be essential for NOB to reduce hypoxia-induced apoptosis of the BeWo cell lines. In summary, NOB attenuated hypoxia-induced placental damage by regulating the P53 signaling pathway, and those findings may contribute some insights into the role of NOB in placental development and the prevention of placental-related diseases.

As the main organelles for the clearance of damaged proteins and damaged organelles, the function of lysosomes is crucial for maintaining the intracellular homeostasis of long-lived neurons. A stable acidic environment is essential for lysosomes to perform their functions. TMEM175 has been identified as a new K+channel that is responsible for regulating lysosomal membrane potential and pH stability in neurons. This study aimed to understand the role of TMEM175 in lysosomal function of neurons and neuronal injury following cerebral ischemia-reperfusion (I/R). A middle-cerebral-artery occlusion/reperfusion (MCAO/R) model was established in adult male Sprague-Dawley rats in vivo, and cultured neurons were exposed to oxygen-glucose deprivation/reoxygenation (OGD/R) to mimic ischemia-reperfusion (I/R) injury in vitro. We found that the protein level of TMEM175 decreased after cerebral I/R injury and that TMEM175 overexpression ameliorated MCAO/R-induced brain-cell death and neurobehavioral deficits in vivo. Furthermore, these results were recapitulated in cultured neurons. Acridine orange (AO) staining, as well as LysoSensor Green DND-189, cathepsin-B (CTSB), and cathepsin-D (CTSD) activities, showed that TMEM175 deficiency inhibited the hydrolytic function of lysosomes by affecting lysosomal pH. In contrast, TMEM175 upregulation reversed OGD/R-induced lysosomal dysfunction and impaired mitochondrial accumulation in cultured neurons. TMEM175 deficiency induced by cerebral I/R injury leads to compromised lysosomal pH stability, thus inhibiting the hydrolytic function of lysosomes. Consequently, lysosomal-dependent degradation of damaged mitochondria is suppressed and thereby exacerbates brain damage. Exogenous up-regulation of TMEM175 protein level could reverse the neuronal lysosomal dysfunction after ischemia-reperfusion.

Hydrogen sulfide (H2S) is recognized to be a novel mediator after carbon monoxide and nitric oxide in the organism. It can be produced in various mammalian tissues and exert many physiological effects in many systems including the cardiovascular system. A great amount of recent studies have demonstrated that endogenous H2S and exogenous H2S-releasing compounds (such as NaHS, Na2S, and GYY4137) provide protection in many cardiovascular diseases, such as ischemia/reperfusion injury, heart failure, cardiac hypertrophy, and atherosclerosis. In recent years, many mechanisms have been proposed and verified the protective role exhibited by H2S against myocardial ischemia/reperfusion injury, and this review is to demonstrate the protective role of exogenous and endogenous H2S on myocardial ischemia/reperfusion injury.

Using Na2B4O7-20%K2CO3 as molten salt, the electrolytic boronizing process was used to prepare TiB whiskers on the surface of the titanium. X-ray diffraction (XRD) and electron probe micro analysis (EPMA) techniques were applied to determine the phases and their contents in boride layer. The cross-section morphology of the boride layer was measured by scanning electron microscope (SEM). The results showed that the boride layer was composed of TiB2 and TiB, with continuous phase TiB2 as the outer layer and TiB whisker as the intermediate layer. The maximum length of TiB whisker could reach 230 µm, with an aspect ratio of over 1,000. The TiB whiskers were embedded into titanium substrate. The hardness of boride increase from 2,049.7 MPa to 3,270.6 MPa.