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1.
Chinese Journal of Biochemical Pharmaceutics ; (6): 303-305, 2017.
Artigo em Chinês | WPRIM | ID: wpr-613875

RESUMO

Objective To investigate the safety and feasibility of Minocycline Hydrochloride Ointment and metronidazole membrane in the treatment of periodontal abscess.Methods80 cases of patients with periodontal abscess in our hospital from May 2014 to May 2016 were selected, these patients were randomly divided into Minocycline Hydrochloride Ointment group (n=40) and metronidazole membrane group (n=40) two groups, the periodontal probing depth, gingival bleeding index, plaque index, attachment loss, clinical efficacy, the incidences of adverse reactions and recurrence of the two groups were statistically analyzed.ResultsThe periodontal probing depth, gingival bleeding index, plaque index, attachment loss of the Minocycline Hydrochloride Ointment group were significantly lower (P<0.05), the total treatment efficiency 95% (38/40) was significantly higher than the metronidazole membrane group 77.5% (31/40) (P<0.05), the recurrence rate 2.5% (1/40) was significantly lower than the metronidazole membrane group 15% (6/40) (P<0.05), but the difference of the incidences of adverse reactions 10% (4/40), 7.5% (3/40) between the two groups was not significant.ConclusionMinocycline Hydrochloride Ointment metronidazole membrane in the treatment of periodontal abscess has higher safety and feasibility than metronidazole membrane, so is worthy of promotion in the clinical.

2.
Chinese Journal of Biochemical Pharmaceutics ; (6): 164-166, 2017.
Artigo em Chinês | WPRIM | ID: wpr-612764

RESUMO

Objective To analyze the anesthetic effect of Compound Articaine on Children's dental pulp without pain, and provide reference for clinical treatment.Methods124 patients with children with dental pulp disease in hospital from February 2015 to May 2016 were selected, patients were randomly divided into observation group and control group, every group with 62 cases.Control group patients were given Lidocaine anesthesia, observation group patients were taken trentment of compound articaine anesthesia, anesthetic effect of patients were compared.Changes in heart rate, blood pressure, adverse effects, and patient pain were recorded before and after anesthesia.ResultsThe total effective rate (96.8%) in the observation group was significantly higher than that in the control group (80.9%) (P<0.05).Observation group (79%) was significantly higher than the control group (1.6%,P<0.05), the observation group of severe pain rate (58.1%) was significantly lower than the control group (11.3%) (P<0.05),The heart rate and blood pressure in the observation group were no significant change, In the control group, the diastolic blood pressure (71.7±10.8) mmHg was significantly lower in the observation group (74.5±12.8) mmHg and the heart rate (80.2±8.8)/min was significantly higher than that in the observation group (76.2±8.3).Two groups of patients in the treatment of adverse reactions, including tachycardia, dizziness, headache, observation group of adverse reaction rate and the control group was not significantly different.ConclusionCompound articaine anesthesia was the implementation of children's dental painless treatment, can reduce the pain of patients, maintain the blood pressure and heart rate stable, has the use value.

3.
Journal of Veterinary Science ; : 63-70, 2016.
Artigo em Inglês | WPRIM | ID: wpr-110764

RESUMO

Gap junctions mediate direct communication between cells; however, toxicological cascade triggered by nonessential metals can abrogate cellular signaling mediated by gap junctions. Although cadmium (Cd) is known to induce apoptosis in organs and tissues, the mechanisms that underlie gap junction activity in Cd-induced apoptosis in BRL 3A rat liver cells has yet to be established. In this study, we showed that Cd treatment decreased the cell index (a measure of cellular electrical impedance) in BRL 3A cells. Mechanistically, we found that Cd exposure decreased expression of connexin 43 (Cx43), increased expression of p-Cx43 and elevated intracellular free Ca2+ concentration, corresponding to a decrease in gap junctional intercellular communication. Gap junction blockage pretreatment with 18β-glycyrrhizic acid (GA) promoted Cd-induced apoptosis, involving changes in expression of Bax, Bcl-2, caspase-3 and the mitochondrial transmembrane electrical potential (Δψm). Additionally, GA was found to enhance ERK and p38 activation during Cd-induced activation of mitogen-activated protein kinases, but had no significant effect on JNK activation. Our results indicated the apoptosis-related proteins and the ERK and p38 signaling pathways may participate in gap junction blockage promoting Cd-induced apoptosis in BRL 3A cells.


Assuntos
Animais , Ratos , Apoptose/efeitos dos fármacos , Cádmio/toxicidade , Cálcio/metabolismo , Comunicação Celular/efeitos dos fármacos , Conexina 43/genética , Ativação Enzimática/efeitos dos fármacos , Junções Comunicantes/efeitos dos fármacos , Regulação da Expressão Gênica/efeitos dos fármacos , Hepatócitos/citologia , Transdução de Sinais/efeitos dos fármacos
4.
Journal of Veterinary Science ; : 151-156, 2015.
Artigo em Inglês | WPRIM | ID: wpr-44467

RESUMO

The purpose of this study was to determine whether the Ca2+ signaling pathway is involved in the ability of osteoprotegerin (OPG) to inhibit osteoclast differentiation and maturation. RAW264.7 cells were incubated with macrophage colony-stimulating factor (M-CSF) + receptor activator of nuclear factor-kappaB ligand (RANKL) to stimulate osteoclastogenesis and then treated with different concentrations of OPG, an inhibitor of osteoclast differentiation. The intracellular Ca2+ concentration [Ca2+]i and phosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) in the different treatment groups were measured by flow cytometry and Western blotting, respectively. The results confirmed that M-CSF + RANKL significantly increased [Ca2+]i and CaMKII phosphorylation in osteoclasts (p < 0.01), and that these effects were subsequently decreased by OPG treatment. Exposure to specific inhibitors of the Ca2+ signaling pathway revealed that these changes varied between the different OPG treatment groups. Findings from the present study indicated that the Ca2+ signaling pathway is involved in both the regulation of osteoclastogenesis as well as inhibition of osteoclast differentiation and activation by OPG.


Assuntos
Animais , Camundongos , Cálcio/metabolismo , Sinalização do Cálcio , Diferenciação Celular/efeitos dos fármacos , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Regulação da Expressão Gênica/efeitos dos fármacos , Fator Estimulador de Colônias de Macrófagos/metabolismo , Osteoclastos/citologia , Osteoprotegerina/farmacologia , Ligante RANK/metabolismo
5.
Journal of Veterinary Science ; : 297-306, 2015.
Artigo em Inglês | WPRIM | ID: wpr-66456

RESUMO

Exposure to cadmium (Cd) induces apoptosis in osteoblasts (OBs); however, little information is available regarding the specific mechanisms of Cd-induced primary rat OB apoptosis. In this study, Cd reduced cell viability, damaged cell membranes and induced apoptosis in OBs. We observed decreased mitochondrial transmembrane potentials, ultrastructure collapse, enhanced caspase-3 activity, and increased concentrations of cleaved PARP, cleaved caspase-9 and cleaved caspase-3 following Cd treatment. Cd also increased the phosphorylation of p38-mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinases (ERK)1/2 and c-jun N-terminal kinase (JNK) in OBs. Pretreatment with the caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, ERK1/2 inhibitor (U0126), p38 inhibitor (SB203580) and JNK inhibitor (SP600125) abrogated Cd-induced cell apoptosis. Furthermore, Cd-treated OBs exhibited signs of oxidative stress protection, including increased antioxidant enzymes superoxide dismutase and glutathione reductase levels and decreased formation of reactive oxygen species. Taken together, the results of our study clarified that Cd has direct cytotoxic effects on OBs, which are mediated by caspase- and MAPK pathways in Cd-induced apoptosis of OBs.


Assuntos
Animais , Ratos , Apoptose/efeitos dos fármacos , Cádmio/toxicidade , Caspases/metabolismo , Poluentes Ambientais/toxicidade , Osteoblastos/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Ratos Sprague-Dawley , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
6.
Journal of Veterinary Science ; : 485-493, 2014.
Artigo em Inglês | WPRIM | ID: wpr-24552

RESUMO

Cadmium (Cd) is a well-known hepatotoxic environmental pollutant. We used rat hepatocytes as a model to study oxidative damage induced by Cd, effects on the antioxidant systems, and the role of N-acetylcysteine (NAC) in protecting cells against Cd toxicity. Hepatocytes were incubated for 12 and 24 h with Cd (2.5, 5, 10 microM). Results showed that Cd can induce cytotoxicity: 10 microM resulted in 36.2% mortality after 12 h and 47.8% after 24 h. Lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase activities increased. Additionally, reactive oxygen species (ROS) generation increased in Cd-treated hepatocytes along with malondialdehyde levels. Glutathione concentrations significantly decreased after treatment with Cd for 12 h but increased after 24 h of Cd exposure. In contrast, glutathione peroxidase activity significantly increased after treatment with Cd for 12 h but decreased after 24 h. superoxide dismutase and catalase activities increased at 12 h and 24 h. glutathione S-transferase and glutathione reductase activities decreased, but not significantly. Rat hepatocytes incubated with NAC and Cd simultaneously had significantly increased viability and decreased Cd-induced ROS generation. Our results suggested that Cd induces ROS generation that leads to oxidative stress. Moreover, NAC protects rat hepatocytes from cytotoxicity associated with Cd.


Assuntos
Animais , Ratos , Acetilcisteína/metabolismo , Antioxidantes/metabolismo , Cádmio/toxicidade , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Poluentes Ambientais/toxicidade , Hepatócitos/efeitos dos fármacos , Estresse Oxidativo , Ratos Sprague-Dawley , Espécies Reativas de Oxigênio/metabolismo
7.
Chinese Journal of Pharmacology and Toxicology ; (6): 1-7, 2010.
Artigo em Chinês | WPRIM | ID: wpr-404275

RESUMO

OBJECTIVE To investigate the potential protective effect of Achyranthes bidentata polysaccharides (ABP) on diabetes mice induced by streptozocin. METHODS Male ICR mice were divided into normal control, diabetes model and ABP 50 and 100 mg·kg~(-1) (ip, once daily for 15 d) treatment groups. On the day before ABP administration and after ABP administration for 8 and 15 d, the blood glucose content was detected with a glucometer and intraperitoneal glucose tolerance test was also conducted. After ABP administration for 15 d, the mice were sacrificed and body weight, heart, liver, spleen and kidneys weights were measured. The serum insulin concentration was determined by radioimmunoassay kit. The serum activities of glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT) and alkaline phosphatase (ALP), and serum concentrations of triglyceride (TG), total cholesterol (TC), calcium and phosphorus were measured by colorimetric method. Enzyme linked immunosorbent assay was employed to detect the concentrations of leptin, adiponectin, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in serum. RESULTS Compared with mice in normal control group, the body weight and serum insulin concentration decreased and blood glucose increased in diabetic model mice. ABP 50 and 100 mg·kg~(-1) treated mice were able to normalize glucose concentrations better following a glucose tolerance test, and the blood glucose level decreased by 27.4% and 16.3%, respectively, compared with that of diabetic model mice. The relative weights of spleen and kidneys, blood glucose level, serum TG and TC concentrations, and GOT, GPT and ALP activities in mice treated with ABP 50 mg·kg~(-1) were obviously lower than those of diabetes model mice. Serum leptin concentration was also markedly decreased near to normal level. However, serum concentrations of adiponectin, TNF-α and IL-6 were significantly increased comparing with diabetes model mice. ABP 100 mg·kg~(-1) had no obvious effect on serum TG and TC levels, and GPT and ALP activities. Its effects on the other parameters indicated above were similar to those in ABP 50 mg·kg~(-1) group. For the serum concentrations of insulin, calcium and phosphorus, no statistical difference could be observed among the different groups. CONCLUSION ABP possesses protective effect against streptozocin-induced diabetes in mice.

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