VIVIAN CURY
Projetos de Pesquisa
Unidades Organizacionais
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- Laser therapy, used in a specific dose, modulates pulmonary inflammatory processes in an experimental model of sepsis in rats(2015) BUBLITZ, Caroline; ASSIS, Livia; RENNÓ, Ana Cláudia M.; CURY, Vivian; HARADA, Gabriela; HIRAI, Aya H.; YAMAUCHI, Liria YuriABSTRACT This study aimed to determine the effectiveness of LLLT in decreasing the lung inflammatory process in septic rats. A total of 32 male Wistar rats were divided into four groups (n=8): control group (CG), sepsis 24h (S24), sepsis and LLLT with 30 J/cm² (S24L30); sepsis and LLLT with 65 J/cm² (S24L65). The irradiation was performed immediately after surgery in the anterior region of the trachea and ventral regions of the chest, bilaterally, just below the ribs. Histological analysis of lung tissue was performed and the number of inflammatory cells was quantified. The S24 group showed an increase of inflammatory cells compared to the CG (p <0.01); S24L30 increased the number of inflammatory cells, while S24L65 decreased this number compared to S24 (both p<0.05); S24L65 had a lower number of inflammatory cells compared to S24L30 (p<0.01). In conclusion, LLLT at a specific energy dose (30J / cm²) was capable of decreasing the number of inflammatory cells in acute lung tissue inflammation due to sepsis.
conferenceObject Effect of low level laser therapy on lung mechanics and inflammatory response(2013) CURY, Vivian; LIMA, Thais; ARIGA, Suely; BARBEIRO, Denise; PINHEIRO, Nathalia; PRADO, Carla Maximo; MORETTI, Ana Iochabel; SOUZA, Heraldo PossoloconferenceObject Effect of low level laser therapy on acute lung injury(2012) CURY, Vivian; LIMA-SALGADO, Thais; PINHEIRO, Natalia; PRADO, Carla Maximo; ASSIS, Livia; MORETTI, Ana Iochabel; SOUZA, Heraldo PossoloLow level laser therapy (LLLT) is prescribed as adjuvant therapy for inflammatory diseases. Hence, we examined whether LLLT may ameliorate acute lung injury (ALI) induced by intratracheal LPS instillation. C57 black mice (n=10 per group) were treated with intratracheal LPS (5mg/kg) or PBS. Six hours after instillation, two groups (PBS and LPS) were irradiated with laser at 660 nm, power output 30mW, fluency 10J/cm2. We observed a marked decrease in the number of cells recovered by bronchoalveolar lavage in LPS + LLLT animals compared to LPS alone (2.0±0.8 x 4.4±1.3, respectively p<0.05). LLLT also decreased the number of inflammatory cells infiltrated in lung interstitium (49.6±3.15 x 71.8±3.92), p<0.05). There was also a decrease in the expression of F4/80 (macrophage surface marker) and MCP-1 (monocyte chemoattractant protein-1), detected by quantitative PCR, in animals submitted to LPS + LLLT, when compared to animals that received only LPS. A marked decrease in cytokines secretion (IL1β, TNFα, IL6, IL10) was also observed in LPS+LLLT group. No difference was observed in animals that received PBS, regardless of LLLT. Therefore, LLLT decreases pulmonary inflammatory cell infiltration, cytokines and chemokines secretion in an experimental model of ALI, supporting the notion that laser therapy attenuates inflammatory intensity, what can contribute to accelerate ALI resolution.- Low-level laser therapy (808 nm) reduces inflammatory response and oxidative stress in rat tibialis anterior muscle after cryolesion(2012) ASSIS, Livia; MORETTI, Ana I. S.; ABRAHAO, Thalita B.; CURY, Vivian; SOUZA, Heraldo P.; HAMBLIN, Michael R.; PARIZOTTO, Nivaldo A.Background and Objective Muscle regeneration is a complex phenomenon, involving coordinated activation of several cellular responses. During this process, oxidative stress and consequent tissue damage occur with a severity that may depend on the intensity and duration of the inflammatory response. Among the therapeutic approaches to attenuate inflammation and increase tissue repair, low-level laser therapy (LLLT) may be a safe and effective clinical procedure. The aim of this study was to evaluate the effects of LLLT on oxidative/nitrative stress and inflammatory mediators produced during a cryolesion of the tibialis anterior (TA) muscle in rats. Material and Methods Sixty Wistar rats were randomly divided into three groups (n?=?20): control (BC), injured TA muscle without LLLT (IC), injured TA muscle submitted to LLLT (IRI). The injured region was irradiated daily for 4 consecutive days, starting immediately after the lesion using a AlGaAs laser (continuous wave, 808?nm, tip area of 0.00785?cm2, power 30?mW, application time 47?seconds, fluence 180?J/cm2; 3.8?mW/cm2; and total energy 1.4?J). The animals were sacrificed on the fourth day after injury. Results LLLT reduced oxidative and nitrative stress in injured muscle, decreased lipid peroxidation, nitrotyrosine formation and NO production, probably due to reduction in iNOS protein expression. Moreover, LLLT increased SOD gene expression, and decreased the inflammatory response as measured by gene expression of NF-k beta and COX-2 and by TNF-a and IL-1 beta concentration. Conclusion These results suggest that LLLT could be an effective therapeutic approach to modulate oxidative and nitrative stress and to reduce inflammation in injured muscle. Lasers Surg. Med. 44: 726735, 2012. (c) 2012 Wiley Periodicals, Inc.
- Inducible nitric oxide synthase inhibition increases MMP-2 activity leading to imbalance between extracellular matrix deposition and degradation after polypropylene mesh implant(2013) SOUZA-PINTO, Franciso J. P.; MORETTI, Ana I. S.; CURY, Vivian; MARCONDES, Wagner; VELASCO, Irineu T.; SOUZA, Heraldo P.Prosthetic mesh implants are commonly used to correct abdominal wall defects. However, success of the procedure is conditioned by an adequate inflammatory response to the device. We hypothesized that nitric oxide produced by nitric oxide synthase 2 (NOS2) and MMP-2 and -9 participate in response induced by mesh implants in the abdominal wall and, consequently, affect the outcome of the surgical procedure. In the first step, temporal inflammatory markers profile was evaluated. Polypropylene meshes were implanted in the peritoneal side of the abdominal wall of C57Black mice. After 2, 4, 7, 15, and 30 days, tissues around the mesh implant were collected and inflammatory markers were analyzed. In the second step, NOS2 activity was inhibited with nitro-L-arginine methyl ester (L-NAME). Samples were collected after 15 days (when inflammation was reduced), and the inflammatory and tissue remodeling markers were investigated. Polypropylene mesh implant induced a pro-inflammatory environment mediated by intense MMP-2 and -9 activities, NO release, and interleukin-1 production peaking in 7 days and gradually decreasing after 15 days. NOS2 inhibition increased MMP-2 activity and resulted in a higher visceral adhesion incidence at the mesh implantation site when compared with non-treated animals that underwent the same procedure. We conclude that NOS2-derived NO is crucial for adequate response to polypropylene mesh implant integration in the peritoneum. NO deficiency results in an imbalance between extracellular matrix deposition/degradation contributing to visceral adhesions incidence. (c) 2012 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2013.
- Nitric oxide modulates metalloproteinase-2, collagen deposition and adhesion rate after polypropylene mesh implantation in the intra-abdominal wall(2012) MORETTI, Ana I. S.; PINTO, Francisco J. P. Souza; CURY, Vivian; JURADO, Marcia C.; MARCONDES, Wagner; VELASCO, Irineu T.; SOUZA, Heraldo P.Prosthetic meshes are commonly used to correct abdominal wall defects. However, the inflammatory reaction induced by these devices in the peritoneum is not completely understood. We hypothesized that nitric oxide (NO), produced by nitric oxide synthase 2 (NOS2) may modulate the response induced by mesh implants in the abdominal wall and, consequently, affect the outcome of the surgical procedure. Polypropylene meshes were implanted in the peritoneal side of the abdominal wall in wild-type and NOS2-deficient (NOS2(-/-)) mice. After 15 days tissues around the mesh implant were collected, and inflammatory markers (the cytokine interleukin 1 beta (IL-1 beta) and NO) and tissue remodeling (collagen and metalloproteinases (MMP) 2 and 9) were analyzed. The lack of NOS2-derived NO induced a higher incidence of visceral adhesions at the mesh implantation site compared with wild-type mice that underwent the same procedure (P < 0.05). Additionally, higher levels of IL-1 beta were present in the mesh-implanted NOS2(-/-) animals compared with control and wild-type mice. Mesh implantation induced collagen I and III deposition, but in smaller amounts in NOS2(-/-) mice. MMP-9 activity after the surgical procedure was similarly increased in both groups. Conversely, MMP-2 activity was unchanged in mesh-implanted wild-type mice, but was significantly increased in NOS2(-/-) mice (P < 0.01), due to decreased S-nitrosylation of the enzyme in these animals. We conclude that NOS2-derived NO is crucial for an adequate response to and integration of polypropylene mesh implants in the peritoneum. NO deficiency results in a prolonged inflammatory reaction to the mesh implant, and reduced collagen deposition may contribute to an increased incidence of visceral adhesions.