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Influência da proteína de choque térmico de 70 kDa de Toxoplasma gondii (TgHSP 70) na modulação da apoptose de células trofoblásticas (Linhagem BeWo)

Fri, 29 May 2015 00:00:00 GMT

Title: Influência da proteína de choque térmico de 70 kDa de Toxoplasma gondii (TgHSP 70) na modulação da apoptose de células trofoblásticas (Linhagem BeWo) Abstract: Toxoplasmosis is an important zoonotic disease due to ability of its causal agent, Toxoplasma gondii, to infect large number of vertebrates and to be associated with congenital infection. Additionally, the parasite requires the heat shock protein of 70 kDa (TgHSP70) for stage conversion. HSP 70 protein displays the ability to modulate various signaling pathways, including the apoptosis by due anti apoptotic mechanisms. Thus, the objective of this study was to investigate the role of heat shock protein of T. gondii (TgHSP 70) on BeWo trophbastic cell line. In order to determine whether TgHSP70 can prevent apoptosis arsenic trioxide (As2O3) and arsenite sodium (NaAs02) were used to induce apoptosis on BeWo and infected with the RH and ME49 strains. To achieve the effect of TgHSP70 on apoptosis, purification and treatment of cells with recombinant TgHSP70 was carried out. Immunocytochemical assay using M30 antibody was performed to evaluated the expression of cytokeratin 18. Also As2O3 was used to induce apoptosis in BeWo cells. This cells their and followed by ME 49 and RH strains infection. The amount of TgHSP 70 expression was evaluated by qPCR analysis. Our results showed that BeWo trophoblastic cells treated with TgHSP 70 protein present lower levels of apoptosis even in the presence of inducers such as NaAsO2 and As2O3. The RH strain of T. gondii has a tendency to modulate apoptosis in BeWo cells compared to cells infected with ME 49 strain. Moreover, our qPCR results revelead that RH strain induces TgHSP70 expression in those cells. Finally, these data suggest that TgHSP70 can be directly associated to the decrease of apoptosis in BeWo cells.

Análise do perfil epidemiológico e clínico dos acidentes ofídicos registrados no Brasil na última década

Mon, 29 Jul 2024 00:00:00 GMT

Title: Análise do perfil epidemiológico e clínico dos acidentes ofídicos registrados no Brasil na última década Abstract: Snakebite is a global public health problem, being considered a Neglected Tropical Disease by the World Health Organization. The dissemination of clinical and epidemiological information on snakebite accidents recorded in Brazil allows us to assess the severity of this public health problem in our country. Objective: To analyze the epidemiological and clinical profile of snakebites recorded in Brazil from 2012 to 2022. Methods: Descriptive and analytical review of epidemiological and clinical characteristics related to snakebites, based on data recorded in SINAN, from 2012 to 2022.The epidemiological analysis of snakebites was carried out based on data recorded in SINAN, from 2012 to 2022. The analysis of data relating to studies on snakebite poisoning found in the medical-scientific literature was carried out through a systematic review, using the PRISMA method. Results and Discussion: 277,394 snakebites were recorded in the country, with an average of 25,217.6 cases per year, of which 80% are caused by snakes of the genus Bothrops and occur predominantly in the North and Northeast regions. We observed a predominance of male victims (77%) and those of economically active age (predominantly in the age group of 20 to 39 years of age, with 34% of cases). These data corroborate the articles studied in this work, and with the literature in general. The epidemiological profile of snakebites recorded in Brazil has remained similar throughout this decade and data on the victims' clinical conditions suggest that, despite the considerable percentage of cases with moderate to severe symptoms, which can culminate in disabling sequelae and even in deaths, the majority of victims received rapid medical care and adequate treatment. The early use of specific antivenom serum for each genus of venomous snake, in the first hours after the victim is bitten by a snake, is decisive for adequate treatment, avoids complications and serious injuries caused by the venoms, and greatly increases the chances of a cure. Conclusion: Snakebites are a non-eradicable problem. Therefore, the union between science and public policies is very important to develop measures to prevent and control snakebite in Brazil. Such measures must consider regional specificities, such as: socioeconomic, educational and cultural level of the population, access to information and specialized medical centers.

Estudo da modulação endógena por óxido nítrico na dor aguda e hiperalgésica inflamatória

Mon, 21 Jul 2025 00:00:00 GMT

Title: Estudo da modulação endógena por óxido nítrico na dor aguda e hiperalgésica inflamatória Abstract: Nitric oxide exerts complex and site-specific modulatory effects on pain signaling pathways. This study evaluated the influence of nitric oxide and nitric oxide synthase inhibition on primary nociceptive neurons in vitro and on nociceptive behavior and inflammatory hyperalgesia in vivo. Cultured rat dorsal root ganglion neurons were exposed to the nitric oxide donor Sodium Nitroprusside (10 μM, 100 μM, 1 mM), and membrane depolarization was assessed via DiBAC4(3) fluorescence. The oxide nitric synthase inhibitor L-NAME was also tested for its impact on capsaicin-induced depolarization and glutamatergic via. Sodium Nitroprusside induced significant depolarization of nociceptive neurons only at 1 mM (0.18 ± 0.02 vs. -0.03 ± 0.005, p < 0.0001), with no effect on capsaicin-induced depolarization. L-NAME alone did not alter resting membrane potential, but potentiated capsaicin-induced depolarization (0.60 ± 0.06 vs. -0.37 ± 0.03, p < 0.001), suggesting a tonic inhibitory role of endogenous nitric oxide. NMDA induced significant depolarization (0.15 ± 0.04 vs. -0.03 ± 0.03, p = 0.03), an effect inhibited by co-administration with L-NAME, indicating nitric oxide-dependent glutamatergic signaling. Intracellular nitric oxide levels were assessed in cultured rat dorsal root ganglion neurons and satellite glial cells using the fluorescent indicator DAF-FM. Cells were exposed to the oxide nitric synthase inhibitor L-NAME and the glutamatergic agonist NMDA to evaluate the contribution of endogenous nitric oxide production to glutamatergic signaling. DAF-FM fluorescence confirmed that L-NAME reduced nitric oxide levels in neurons (-0.44 ± 0.09 vs. 0.11 ± 0.01, p < 0.0001) and satellite glial cells (-0.5 ± 0.09 vs. 0.7 ± 0.01, p < 0.0001). NMDA increased NO levels in neurons (0.11 ± 0.02 vs. -0.72 ± 0.02, p = 0.007) and in SGCs (0.08 ± 0.04 vs. -0.7 ± 0.02, p < 0.0001), and this response was inhibited in the presence of L-NAME. In vivo, L-NAME was administered through intraperitoneal, intraplantar, intrathecal and intraganglionic injections prior to nociceptive stimuli with capsaicin or to carrageenan-induced inflammation. Behavioral nociceptive responses and mechanical hypersensitivity thresholds were measured to assess acute pain and hyperalgesia. Systemic administration of L-NAME increased acute nociceptive responses (64.1 ± 5.3 vs. 40.6 ± 4.7, p < 0.01) with no effect on inflammatory hyperalgesia. Local administration reduced both acute nociception (49.8 ± 2.0 vs. 82.7 ± 4.1, p < 0.0001) and hyperalgesia, both at 1h30 (41.5 ± 3.0 vs. 17.4 ± 2.5, p < 0.002) and 3h (44.9 ± 0.8 vs. 32.9 ± 1.9, p < 0.0001). Spinal administration enhanced acute nociceptive responses (50.7 ± 2.8 vs. 36.2 ± 3.5, p < 0.008) and reduced hyperalgesia (53.3 ± 11.1 vs. 34.0 ± 5.4, p < 0.0001). Intraganglionic injection did not affect acute nociception but reduced inflammatory hyperalgesia (44.0 ± 0.8 vs. 32.8 ± 1.8, p < 0.003), indicating that ganglionic nitric oxide signaling contributes to the maintenance of mechanical hypersensitivity. These data support a dual and compartmentalized role for nitric oxide in pain modulation, acting facilitatively at peripheral sites and tonically inhibiting nociceptive signaling centrally. Understanding the spatially distinct actions of nitric oxide provides insight into its complex involvement in pain processing and highlights the importance of targeted approaches for therapeutic modulation of nitric oxide pathways.

As células trofoblásticas de glicogênio murinas estão associadas à restrição do crescimento fetal em malária gestacional

Thu, 27 Feb 2025 00:00:00 GMT

Title: As células trofoblásticas de glicogênio murinas estão associadas à restrição do crescimento fetal em malária gestacional Abstract: Gestational malaria, caused by Plasmodium infection during pregnancy, leads to severe complications such as anemia and low birth weight. The placenta plays a crucial role in fetal development by producing hormones, supplying nutrients and oxygen, and providing protection against infections. This study aimed to investigate the impact of Plasmodium berghei NK65GFP (PbNK65) infection on placental function and fetal growth in two mouse strains: C57BL/6 and BALB/c. To this end, pregnant female mice of both strains were infected with PbNK65 at gestational day 9.5 and analyzed at gestational day 16.5. Parasitemia was assessed over a time course. Fetal weight and placental weight were measured at day 16.5 of gestation (7 days post-infection), along with placental glycogen levels using PAS staining, and levels of glucagon, protocadherin 12 (Pcdh12), Ki-67, and matrix metalloproteinase-9 (MMP-9) in the uterus/placenta by immunohistochemistry. The results showed that PbNK65 infection led to significant reductions in placental glycogen content and fetal weight in both mouse strains. Uninfected C57BL/6 mice exhibited higher placental glycogen storage compared to uninfected BALB/c mice. However, infection caused a decrease in glycogen storage in both strains, with a greater impact observed in BALB/c mice. Glucagon and Pcdh12 expression were increased in the placental tissues of infected BALB/c animals, while remaining unchanged or decreased, respectively, in C57BL/6 mice, suggesting a potential adaptive response to infection. The infection also increased MMP-9 levels in the placentas of C57BL/6 animals, and these levels were higher in C57BL/6 mice compared to BALB/c mice. In conclusion, both mouse strains showed reduced glycogen storage and fetal weight under PbNK65 infection. However, BALB/c fetuses exhibited less weight loss compared to the C57BL/6 strain, which was associated with higher levels of glucagon and Pcdh12 in the placental tissues of BALB/c mice. These findings suggest that glycogen storage and glycogen trophoblast cells play a role in maintaining fetal weight during gestational malaria, and that increased MMP-9 abundance in the placentas of C57BL/6 mice indicates an inflammatory response that may negatively impact gestational health. Keywords: Gestational malaria; Plasmodium berghei NK65; glycogen trophoblast cells; glycogen storage; fetal weight.