Acta cirurgica brasileira最新文献

Purpose: Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers with increasing incidence. Even if progress have been made, the five-year overall survival remains lower than 10%. There is a desperate need in therapeutic improvements. In the last two decades, new in-vitro models have been developed and improved, including tridimensional-culture spheroids and organoids. However, animal studies remain mandatory in the upscaling before clinical studies. Orthotopic and syngeneic grafting is a robust model to test a drug efficiency in a tumor and its microenvironment.

Methods: We described a method for orthotopic and syngeneic graft of KRAS mutated, p53 wildtype, 8305 cells in a C57BL/6J mouse model.

Results: With this microsurgical method, 30 mice were grafted, 24 by a junior and six by a senior, resulting in 95,8 and 100% of (partial and total) successful tumoral implantation, respectively. Twenty mice underwent ultrasound follow-up. It was an efficient method for the tumoral growth evaluation. At day 16 after grafting, 85% of the tumors were detectable by ultrasound, and at day 22 all tumors were detected.

Conclusions: The presented method appears to be a robust and reliable method for pre-clinical studies. A junior master student can provide positive results using this technique, which can be improved with training.

Purpose: To create three-dimensional anatomical models of the thoracic and lumbar portions of the canine spine that reproduce the vertebral surgical approaches of dorsal laminectomy and hemilaminectomy, and to perform the respective radiographic evaluations of each approach.

Methods: In a digital archive of the canine spine, digitally replicate the dorsal laminectomy and hemilaminectomy in the thoracic and lumbar portions and, then, make tridimensional prints of the vertebral models and obtain radiographs in three dorsoventral, ventrodorsal and laterolateral projections.

Results: The anatomical models of the surgical spinal canal accesses of the thoracic and lumbar portions showed great fidelity to the natural bones. The created accesses have the proper shape, location and size, and their radiographic images showed similar radiodensities.

Conclusions: The replicas of the dorsal laminectomy and hemilaminectomy developed in the anatomical models in the thoracic and lumbar portions are able to represent the technical recommendations of the specialized literature, as well as their respective radiographic images, which have certain radiological properties that allow to make a deep radiological study. Therefore, the models are useful for neurosurgical training.

[This corrects the article doi: 10.1590/acb371002].

Purpose: Myocardial ischemia/reperfusion injury (MIRI) leads to myocardial tissue necrosis, which will increase the size of myocardial infarction. The study examined the protective effect and mechanism of the Guanxin Danshen formula (GXDSF) on MIRI in rats.

Methods: MIRI model was performed in rats; rat H9C2 cardiomyocytes were hypoxia-reoxygenated to establish a cell injury model.

Results: The GXDSF significantly reduced myocardial ischemia area, reduced myocardial structural injury, decreased the levels of interleukin (IL-1β, IL-6) in serum, decreased the activity of myocardial enzymes, increased the activity of superoxide dismutase (SOD), and reduced glutathione in rats with MIRI. The GXDSF can reduce the expression of nucleotide- binding oligomerization domain, leucine-rich repeat and pyrin domain containing nod-like receptor family protein 3 (NLRP3), IL-1β, caspase-1, and gasdermin D (GSDMD) in myocardial tissue cells. Salvianolic acid B and notoginsenoside R1 protected H9C2 cardiomyocytes from hypoxia and reoxygenation injury and reduced the levels of tumor necrosis factor α (TNF-α) and IL-6 in the cell supernatant, decreasing the NLRP3, IL-18, IL-1β, caspase-1, and GSDMD expression in H9C2 cardiomyocytes. GXDSF can reduce the myocardial infarction area and alleviate the damage to myocardial structure in rats with MIRI, which may be related to the regulation of the NLRP3.

Conclusions: GXDSF reduces MIRI in rat myocardial infarction injury, improves structural damage in myocardial ischemia injury, and reduces myocardial tissue inflammation and oxidative stress by lowering inflammatory factors and controlling focal cell death signaling pathways.

Purpose: Stroke is an acute cerebrovascular disease. Astragaloside IV (AS-IV) is an active ingredient extracted from Astragalus membranaceus with an established therapeutic effect on central nervous system diseases. This study examined the neuroprotective properties and possible mechanisms of AS-IV in stroke-triggered early brain injury (EBI) in a rat transient middle cerebral artery occlusion (MCAO) model.

Methods: The neurological scores and brain water content were analyzed. 2,3,5-triphenyl tetrazolium chloride (TTC) staining was utilized to determine the infarct volume, neuroinflammatory cytokine levels, and ferroptosis-related genes and proteins, and neuronal damage and molecular mechanisms were evaluated by terminal deoxynucleotidyl transferase dutp nick-end labeling (TUNEL) staining, western blotting, and real-time polymerase chain reaction.

Results: AS-IV administration decreased the infarct volume, brain edema, neurological deficits, and inflammatory cytokines TNF-α, interleukin-1β (IL-1β), IL-6, and NF-κB, increased the levels of SLC7A11 and glutathione peroxidase 4 (GPX4), decreased lipid reactive oxygen species (ROS) levels, and prevented neuronal ferroptosis. Meanwhile, AS-IV triggered the Nrf2/HO-1 signaling pathway and alleviated ferroptosis due to the induction of stroke.

Conclusions: Hence, the findings of this research illustrate that AS-IV administration can improve delayed ischemic neurological deficits and decrease neuronal death by modulating nuroinflammation and ferroptosis via the Nrf2/HO-1 signaling pathway.

[This corrects the article doi: 10.1590/acb371101].

[This corrects the article doi: 10.1590/acb370508].

[This corrects the article doi: 10.1590/acb370705].

Purpose: To analyze the effects of Anacardium occidentale Linn on the healing of skin wounds.

Methods: Twenty Wistar male rats were distributed into four groups (with five animals each one): negative control group (NCG), treated with saline solution; cashew tree group (CG), treated with hydroalcoholic extract of the bark of A. occidentale Linn; manipulated cashew tree group (MCG), with the ointment of extract of the bark of A. occidentale Linn; positive control group (PCG), treated with sunflower oil. All animals were examined daily, observing the macroscopic aspects of the surgical wound. Hematoxylin-eosin staining was used for tissue morphology analysis and Masson's trichrome for better collagen fiber characterization.

Results: On day 7, the MCG group had the expansion of the surgical wound covered by crust, exceeding the initial limits. On day 21, the wounds were observed to be completely closed and epithelialized in the NCG and CG groups. PCG and MCG still had remnants of crusts on the wound. The NCG was the only one not to present an abscess in histopathological analysis.

Conclusions: There was a prolongation of the healing phase of the animals treated with the extract, and the animals in the NCG showed a better outcome by histological analysis.

Purpose: Colorectal cancer (CRC) is a common human cancer along with higher incidence and mortality, and this study aimed to identify the effect of cincumol on CRC and its potential mechanisms.

Methods: CRC cell line HCT116 was used as the material. Cell proliferation was evaluated by CCK-8 assay, and cell migration was detected by scratch test and Transwell assay. TUNEL staining assay was used to evaluate cell apoptosis. The expression of target genes was detected by qualitative real-time polymerase chain reaction and western blot assays.

Results: Cincumol significantly reduced the proliferative and migratory rate and enhanced apoptotic rate of HCT116 cells. Meanwhile, the elevated levels of RBUsuh, Nicd and Tace was also observed in cincumol-treated HCT116 cells. Moreover, our findings revealed that additional cincumol inhibited the expression of p-PI3K and p-AKT, suggesting the inhibition of PI3K/AKT signaling might be involved in the protective role of cincumol on the malignant phenotypes of CRC cells in vitro.

Conclusions: Cincumol inhibited the malignant phenotypes of CRC cells in vitro through inactivating PI3K/AKT signaling, suggesting that cincumol might be a potential anti-CRC agent.