Abstract Objective To investigate the effects of intro-oral injection of parathyroid hormone (PTH) on tooth extraction wound healing in hyperglycemic rats. Methodology 60 male Sprague-Dawley rats were randomly divided into the normal group (n=30) and DM group (n=30). Type 1 diabetes mellitus (DM) was induced by streptozotocin. After extracting the left first molar of all rats, each group was further divided into 3 subgroups (n=10 per subgroup), receiving the administration of intermittent PTH, continuous PTH and saline (control), respectively. The intermittent-PTH group received intra-oral injection of PTH three times per week for two weeks. A thermosensitive controlled-release hydrogel was synthesized for continuous-PTH administration. The serum chemistry was determined to evaluate the systemic condition. All animals were sacrificed after 14 days. Micro-computed tomography (Micro-CT) and histological analyses were used to evaluate the healing of extraction sockets. Results The level of serum glucose in the DM groups was significantly higher than that in the non-DM groups (p<0.05); the level of serum calcium was similar in all groups (p>0.05). Micro-CT analysis showed that the DM group had a significantly lower alveolar bone trabecular number (Tb.N) and higher trabecular separation (Tb.Sp) than the normal group (p<0.05). The histological analyses showed that no significant difference in the amount of new bone (hard tissue) formation was found between the PTH and non-PTH groups (p>0.05). Conclusions Bone formation in the extraction socket of the type 1 diabetic rats was reduced. PTH did not improve the healing of hard and soft tissues. The different PTH administration regimes (continuous vs. intermittent) had similar effect on tissue healing. These results demonstrated that the metabolic characteristics of the hyperglycemic rats produced a condition that was unable to respond to PTH treatment.

ABSTRACT Celosia argentea L., Amaranthaceae, is widely used as traditional medicine with a long history in China. It is a unique source of Semen Celosiae whose contributions include purging the hepatic pathogenic fire, improving eyesight, and treating other eye diseases. Over 79 compounds from this plant were isolated and identified, mainly including saponins, peptides, phenols, fatty acids, and amino acids, of which saponins have been considered as the characteristic and active constituents of Celosia argentea. Experimental evidences manifested that Celosia argentea, with its active compounds, possesses wide-reaching biological activities such as hepatoprotection, tumor treatment, anti-diarrhea, anti-diabetes, anti-oxidant, anti-hypertension, and for treatment of a number of eye diseases. The objective of the study was to provide an overview of the ethno-pharmacology, chemical constituents, pharmacology, and related clinical applications of Celosia argentea, and to reveal their therapeutic potentials, and secure an evidence base for further research works on Celosia argentea.

ABSTRACT Safflower (Carthamus tinctorius L., Asteraceae) is an important oil crop and medicinal plant. Gene expression analysis is gaining importance in the research of safflower. Quantitative PCR has become a powerful method for gene study. Reference genes are one of the major qualification requirements of qPCR because they can reduce the variability. To identify the reference genes in safflower, nine candidate genes of the housekeeping genes were selected from the EST library of safflower constructed by our lab: CtACT (actin), CtGAPDH (glyceraldehyde 3-phosphate dehydrogenase), CtE1F4A (elongation factor 1 alpha), CtTUA (alpha-tubulin), CtTUB (beta-tubulin), CtPP2A (serine/threonine-protein phosphatase), CtE1F4A (eukaryotic initiation factor 4A), CtUBI (Ubiquitin), and Ct60S (60S acidic ribosomal protein). Expression stability was examined by qPCR across 54 samples, representing tissues at different flowering stages and two chemotype of safflower lines. We assessed the expression stability of these candidate genes by employing four different algorithms (geNorm, NormFinder, ΔCt approach, and BestKeeper) and found that CtUBI and Ct60S were the highly ranked candidate genes. CtUBI and Ct60S were used as reference genes to evaluate the expression of CtFAD2-10 and CtKASII. Our data suggest CtUBI and Ct60S could be used as internal controls to normalize gene expression in safflower.

Parkinson’s disease is a chronic neurodegenerative condition affecting elderly persons. In a minority of cases the disease has a genetic origin, but in most the cause is idiopathic. Accumulation of free radicals and loss of glutathione homeostasis have been pointed at as possible causal agents. The purpose of the study was to review experimental evidence supporting the involvement of free radicals and loss of glutathione homeostasis in the outset and progress of substantia nigra pars compacta degeneration. Oxidative stress in Parkinson’s disease may be related to the intrinsic pro-oxidant properties of dopamine and high iron concentrations in the substantia nigra pars compacta, promoting dopamine oxidation and the generation of reactive oxygen species. Any event triggering these mechanisms will cause cell damage. Glutathione reduction is one of the earliest biochemical alterations detected in association with Parkinson’s disease, and it has been related to the inhibition of complex I of the mitochondrial transport chain, oxidative damage and glial activation, among other factors leading to neurodegeneration. This evidence points to the need to maintain glutathione homeostasis in the dopaminergic system, as well as its relationship to the etiology of nigrostriatal degeneration, of potential application in clinical practice.

La enfermedad de Parkinson es una enfermedad neurodegenerativa crónica que afecta a las personas de la tercera edad. En una minoría de los casos la enfermedad es de origen genético pero en el resto, la causa es idiopática. En este sentido, la acumulación de los radicales libres y la pérdida de la homeostasis del glutatión se han señalado como posibles agentes causales. El presente texto se propuso revisar las evidencias experimentales que apoyan la participación de los radicales libres y la pérdida de la homeostasis del glutatión en el comienzo y la progresión de la degeneración de la substantianigrapars compacta. El estrés oxidativo en la enfermedad de Parkinson´s puede estar relacionado con las propiedades pro-oxidantes intrínsecas de la dopamina y elevadas concentraciones de hierro en la substantianigrapars compacta, que promueven la oxidación de la dopamina y la generación de especies reactivas del oxígeno. Cualquier evento que desencadene estos mecanismos, genera un daño celular. La disminución del glutatión es una de las alteraciones bioquímicas más tempranas, detectadas en asociación con la enfermedad de Parkinson y se ha relacionado con la inhibición del complejo I de la cadena de transporte mitocondrial, daño oxidativo, activación glial, entre otros que favorecen la neurodegeneración. Estas evidencias sugieren la necesidad de mantener la homeostasis del glutatión en el sistema dopaminérgico y su vínculo con la etiología de la degeneración nigro-estriatal, lo que tiene una potencial aplicación en la práctica clínica.

Glutathione is an important cellular antioxidant whose depletion leads to oxidative damage and alters short- and long-term synaptic interactions. Taking into account that the role of this molecule in learning and memory has been poorly studied, the present work evaluates the effect of the administration of L-buthionine sulfoximine (BSO) on glutathione content and markers of cellular oxidative damage (malondialdehyde, superoxide dismutase, glutathione peroxidase). BSO was delivered into the brain by intraventricular injection in the frontal cortex, hippocampus and striatum, evaluating the effect of the resulting glutathione depletion on learning and memory by means of the passive avoidance test, performed 7 days after administration. The results suggest that injecting L-buthionine sulfoximine unbalances the antioxidant enzyme system, resulting in damage to cellular lipid components. In addition, the data suggest the existence of a relationship between oxidative damage originated by glutathione depletion and memory consolidation.

El glutatión es un importante antioxidante celular, cuya disminución promueve el daño oxidativo y altera las interacciones sinápticas, a corto y a largo plazo. Su función en el aprendizaje y la memoria ha sido poco estudiada. Se decidió determinar el efecto de la administración del L-butionin sulfoximina sobre el contenido de glutatión, y los indicadores de daño oxidativo celular (malonildialdhehído, superóxido dismutasa, glutatión peroxidasa), a los siete días de la inyección intracerebroventricular, en la corteza frontal, el hipocampo y el cuerpo estriado, así como el efecto de la disminución del glutatión en el aprendizaje y la memoria, mediante la prueba de evitación pasiva. Los resultados sugirieron que el L-butionin sulfoximina induce un desbalance en la actividad enzimática antioxidante, que genera un daño en los componentes lipídicos celulares, y que existe un vínculo entre el daño oxidativo originado por la disminución de glutatión y la consolidación de la memoria.