Changes related to muscle autophagy after exhaustive exercise and blunt trauma / Cambios relacionados con la autofagia muscular tras ejercicio exhaustivo y traumatismo contuso / Alterações relacionadas à autofagia muscular após exercício exaustivo e trauma contuso

ABSTRACT Objective: To study the temporal changes of autophagy related factors in skeletal muscle of rats after exhaustive exercise and blunt trauma. Methods: Forty-two male SD rats were divided into 7 groups with 6 rats in each group: Quiet control group (C), immediately after exhaustive exercise (E0), 24 hours after exhaustive exercise (E24), 48 hours after exhaustive exercise (E48), immediately after blunt trauma (D0), 24 hours after blunt trauma (D24), 48 hours after blunt trauma (D48). All groups of rats were killed and samped respectively at different time points specified above, and the right gastrocnemius muscle was taken, which was divided into two parts, one for mRNAs of, Lamp-2, BNIP3 and NIX by real-time fluorescent quantitative PCR, and the other for p62 protein by Western blotting. Results: (1) Compared with group C, mRNA levels of p62, Lamp-2 and NIX in group E48 were significantly increased after exhaustive exercise(P<0.05), suggesting that autophagy increased in 48h after exhaustive exercise. (2) Compared with group C, p62mRNA and Lamp-2 mRNA levels were significantly increased immediately after blunt trauma(P<0.05) and decreased significantly in 48h after blunt trauma(P<0.05), suggesting that autophagy activity was enhanced immediately after blunt trauma and decreased in 48h after injury. Conclusions: Generally, there were differences at each recovery phase between blunt trauma and exhausted exercise models, and the basal autophagy factors and mitochondrial autophagy factors were also inconsistent. Basal autophagy factors p62 and Lamp-2 increased significantly 48 hours after eccentric exhaustive exercise and immediately after blunt trauma. Mitochondrial autophagy factor BNIP3 did not increase after exhaustive exercise and blunt trauma, but NIX only increased after exhaustive exercise. Its molecular mechanism needs to be further studied. Level of Evidence III; Therapeutic Studies Investigating the Results of Treatment.

RESUMEN Objetivo: Estudiar los cambios temporales de los factores relacionados con la autofagia en el músculo esquelético de ratas tras el ejercicio exhaustivo y el traumatismo contuso. Métodos: Se dividieron 42 ratas SD macho en 7 grupos con 6 ratas en cada grupo: grupo de control silencioso (C), inmediatamente después del ejercicio exhaustivo (E0), 24 horas después del ejercicio exhaustivo (E24), 48 horas después del ejercicio exhaustivo (E48), inmediatamente después de un traumatismo contuso (D0), 24 horas después de un traumatismo contuso (D24), 48 horas después de un traumatismo contuso (D48). Todos los grupos de ratas fueron sacrificados y rotulados, respectivamente, en diferentes momentos especificados anteriormente, y se extrajo el músculo gastrocnemio derecho, dividido en dos partes, una para los ARNm Lamp-2, BNIP3 y NIX mediante PCR cuantitativa fluorescente en tiempo real, y la otra para la proteína p62 mediante Western blotting. Resultados: (1) En comparación con el grupo C, los niveles de ARNm de p62, Lamp-2 y NIX en el grupo E48 aumentaron significativamente tras el ejercicio exhaustivo (P<0,05), lo que sugiere que la autofagia aumentó en las 48 horas posteriores al ejercicio exhaustivo. (2) En comparación con el grupo C, los niveles de ARNm de p62 ARNm y Lamp-2 aumentaron significativamente inmediatamente después del traumatismo contuso (P<0,05) y disminuyeron significativamente a las 48 horas después del traumatismo contuso (P<0,05), lo que sugiere que la actividad de autofagia aumentó inmediatamente después del traumatismo contuso y disminuyó a las 48 horas después de la lesión. Conclusión: En general, hubo diferencias en cada fase de recuperación entre los modelos de traumatismo contuso y ejercicio exhaustivo, y los factores de autofagia basal y los factores de autofagia mitocondrial también fueron inconsistentes. Los factores de autofagia basal p62 y Lamp-2 aumentaron significativamente 48 horas después del ejercicio excéntrico exhaustivo e inmediatamente después del traumatismo contuso. El factor de autofagia mitocondrial BNIP3 no aumentó tras el ejercicio exhaustivo y el traumatismo contuso, pero NIX sólo aumentó tras el ejercicio exhaustivo. Su mecanismo molecular debe investigarse con más detalle. Nivel de Evidencia III; Estudios Terapéuticos que Investigan los Resultados del Tratamiento.

RESUMO Objetivo: Estudar as alterações temporais dos fatores relacionados à autofagia no músculo esquelético de ratos após exercício exaustivo e trauma contuso. Métodos: Quarenta e dois ratos machos SD foram divididos em 7 grupos com 6 ratos em cada grupo: Grupo de controle silencioso (C), imediatamente após o exercício exaustivo (E0), 24 horas após o exercício exaustivo (E24), 48 horas após o exercício exaustivo (E48), imediatamente após o trauma contuso (D0), 24 horas após o trauma contuso (D24), 48 horas após o trauma contuso (D48). Todos os grupos de ratos foram mortos e rotulados, respectivamente, em diferentes momentos especificados acima, e o músculo gastrocnêmio direito foi retirado, dividido em duas partes, uma para mRNAs de Lamp-2, BNIP3 e NIX por PCR quantitativo fluorescente em tempo real, e a outra para a proteína p62 por imunotransferência. Resultados: (1) Em comparação com o grupo C, os níveis de mRNA de p62, Lamp-2 e NIX no grupo E48 aumentaram significativamente após o exercício exaustivo (P<0,05), sugerindo que a autofagia aumentou em 48 horas após o exercício exaustivo. (2) Em comparação com o grupo C, os níveis de mRNA de p62mRNA e Lamp-2 foram significativamente aumentados imediatamente após o trauma contuso (P<0,05) e diminuíram significativamente em 48 horas após o trauma contuso (P<0,05), sugerindo que a atividade de autofagia foi aumentada imediatamente após o trauma contuso e diminuiu em 48 horas após a lesão. Conclusão: Houve, via de regra, diferenças em cada fase de recuperação entre os modelos de trauma contuso e de exercício exaustivo, sendo que os fatores de autofagia basal e os fatores de autofagia mitocondrial também foram inconsistentes. Os fatores de autofagia basal p62 e Lamp-2 aumentaram significativamente 48 horas após o exercício excêntrico exaustivo e imediatamente após o trauma contuso. O fator de autofagia mitocondrial BNIP3 não aumentou após o exercício exaustivo e o trauma contuso, mas o NIX aumentou somente após o exercício exaustivo. Seu mecanismo molecular precisa ser investigado com mais detalhes. Nível de Evidência III; Estudos Terapêuticos que Investigam os Resultados do Tratamento.

Experimental periodontitis induced hypoadiponectinemia by IRE1α-mediated endoplasmic reticulum stress in adipocytes.

BACKGROUD: Hypoadiponectinemia is the important cause of insulin resistance. Recent studies have shown that periodontitis is associated with hypoadiponectinemia. The purpose of this study was to investigate the effect of periodontitis-induced endoplasmic reticulum stress (ERS) in visceral adipocytes on hypoadiponectinemia. METHODS: Rat periodontitis models were established by local ligation with silk around the bilateral maxillary second molars. Porphyromonas gingivalis-lipopolysaccharid (P.g-LPS) was also used to stimulate the visceral adipocytes in vitro. The protein expression levels of glucose regulated protein 78 (GRP78), inositol-requiring protein 1α (IRE1α), protein kinase RNA-like ER kinase (PERK), activating transcription factor 6 (ATF6) and adiponectin were detected. IRE1α lentiviruses were transfected into visceral adipocytes in vitro, and an IRE1α inhibitor (KIRA6) was injected in epididymal adipose tissue of rats to detect and verify the effect of ERS on adiponectin expression in visceral adipocytes in vivo. RESULTS: Hypoadiponectinemia was observed in periodontitis rat, and the expression levels of ERS key proteins GRP78 and the phosphorylation levels of IRE1α (p-IRE1α)/IRE1α in visceral adipocytes were increased, while the expression levels of adiponectin protein were decreased. After KIRA6 injection into epididymal adipose tissue of rats with periodontitis, adiponectin levels in visceral adipocytes increased, and serum adiponectin levels recovered to a certain extent. The protein expression levels of GRP78 and p-IRE1α/IRE1α were increased and adiponectin protein expression was decreased in P.g-LPS-induced visceral adipocytes. Overexpression of IRE1α further inhibited adiponectin expression in P.g-LPS-stimulated visceral adipocytes, and conversely, IRE1α inhibition restored adiponectin expression. CONCLUSIONS: Our findings suggest that periodontitis induces ERS in visceral adipocytes leading to hypoadiponectinemia. IRE1α is a key protein regulating adiponectin expression in visceral adipocytes.

Chronic periodontitis induces the proliferation of pancreatic ß-cells to cause hyperinsulinemia in a rat model.

BACKGROUND AND OBJECTIVE: The purpose of this study was to determine if chronic periodontitis (CP) may induce hyperinsulinemia and may have the effect of on pancreatic ß-cell proliferation in a rat model. MATERIALS AND METHODS: Twelve male Sprague-Dawley rats were divided into two groups: the CP group and the control group (Con group). The following contents were evaluated: pathological changes in periodontal soft and hard tissues; serum lipopolysaccharide (LPS) level, serum fasting insulin (FINS) level, fasting blood glucose (FBG) level, and homeostasis model assessment (HOMA) ß (HOMA-ß) index; histopathological examination of islets; immunohistochemistry of insulin and p-Smad2 expression in islets; immunofluorescence of changes in the relative number of ß-cells and the number of Ki67-positive ß-cells. Western blotting was used to analyze p-Smad2/Smad2 levels. Results were analyzed by two independent samples t tests. RESULTS: Increased serum LPS level, FINS level, and HOMA-ß index were observed in the rats of the CP group; FBG level did not change significantly; histological assessments showed an enlarged islet area, increased insulin content, relatively increased ß-cells, increased Ki67-positive ß-cells, and decreased p-Smad2 expression in islets in the rats of the CP group. CONCLUSION: Our study results link CP-induced hyperinsulinemia with changes in islets, such as islet hyperplasia and compensatory ß-cell proliferation, by using a CP rat model.

Periodontitis as a promoting factor of T2D: current evidence and mechanisms.

Periodontitis is an infectious disease caused by an imbalance between the local microbiota and host immune response. Epidemiologically, periodontitis is closely related to the occurrence, development, and poor prognosis of T2D and is recognized as a potential risk factor for T2D. In recent years, increasing attention has been given to the role of the virulence factors produced by disorders of the subgingival microbiota in the pathological mechanism of T2D, including islet ß-cell dysfunction and insulin resistance (IR). However, the related mechanisms have not been well summarized. This review highlights periodontitis-derived virulence factors, reviews how these stimuli directly or indirectly regulate islet ß-cell dysfunction. The mechanisms by which IR is induced in insulin-targeting tissues (the liver, visceral adipose tissue, and skeletal muscle) are explained, clarifying the influence of periodontitis on the occurrence and development of T2D. In addition, the positive effects of periodontal therapy on T2D are overviewed. Finally, the limitations and prospects of the current research are discussed. In summary, periodontitis is worthy of attention as a promoting factor of T2D. Understanding on the effect of disseminated periodontitis-derived virulence factors on the T2D-related tissues and cells may provide new treatment options for reducing the risk of T2D associated with periodontitis.

Effects of contusion and exhaustive exercise on murf1 and mafbx in the skeletal muscle of rats / Efectos de la contusión y del ejercicio exhaustivo sobre murf1 y mafbx en el músculo esquelético de ratas / Efeitos do trauma contuso e do exercício exaustivo no em murf1 e mafbx no músculo esquelético de ratos

ABSTRACT Objective To study the effects of contusion and exhaustive exercise on the expression of degradation-related factors MuRF1 and MAFbx in the skeletal muscle of rats and describe the repair mechanism of skeletal muscle injury. Methods Forty-two male SD rats were randomly divided into 7 groups. The rats in each group were killed at different time points (0h, 24h, 48h) after exhaustive exercise (E0, E24, E48) and contusion (D0, D24, D48), respectively, and in the resting state in control group (C). The right gastrocnemius muscles were resected and divided into two parts, one for the mRNAs of MuRF1 and MAFbx by real-time PCR, and the other for protein measurement by Western blotting. Results Compared with the control group, the MuRF1 mRNA and protein expression of the skeletal muscle in the E0 group was markedly increased (P <0.05) and followed by a downward trend in E24 the E48 groups. On the other hand, MuRF1 mRNA expression of the skeletal muscle in the D24 group was significantly upregulated (P <0.01), then decreased in the D48 group (P <0.01). Meanwhile, compared with the C group, MAFbx mRNA gene expression continued to be upregulated in D24 and D48 (P <0.05), but decreased in E24 and E48 (p<0.01). On the other hand, the NF-κB protein contents of the skeletal muscle in the D0, D24, and D48 groups, as well as in the E48 group, were markedly downregulated (P <0.05), and the one in E48 was also remarkably downregulated (P <0.05). Conclusion NF-κB may negatively regulate the process of protein degradation by the NF-κB / MuRF1 signal pathway. Level of evidence III; Therapeutic studies investigating the results of treatment.

RESUMEN Objetivo Estudiar los efectos de la contusión y del ejercicio exhaustivo sobre la expresión de los factores relacionados con la degradación MuRF1 y MAFbx en el músculo esquelético de ratas y describir el mecanismo de reparación de la lesión muscular esquelética. Métodos Cuarenta y dos ratas macho SD fueron divididas aleatoriamente en 7 grupos. Las ratas de cada grupo fueron sacrificadas en diferentes momentos (0h, 24h, 48h) después del ejercicio exhaustivo (E0, E24, E48) y de la contusión (D0, D24, D48), respectivamente, y en estado de reposo en el grupo de control (C). Se resecaron los músculos gastrocnemios derechos y se dividieron en dos partes, una para los ARNm de MuRF1 y MAFbx mediante PCR en tiempo real y la otra para la medición de proteínas mediante Western blot. Resultados En comparación con el grupo control, el ARNm de MuRF1 y la expresión proteica del músculo esquelético en el grupo E0 se incrementó notablemente (P <0,05) y fueron seguidos por una tendencia a la baja en los grupos E24 y E48. Por otra parte, la expresión del ARNm de MuRF1 del músculo esquelético en el grupo D24 fue significativamente regulada al alza (P <0,01), y luego disminuyó en el grupo D48 (P <0,01). Mientras tanto, en comparación con el grupo C, la expresión génica del ARNm de MAFbx permaneció regulada al alza en D24 y D48 (P <0,05), pero disminuyó en E24 y E48 (p<0,01). Por otro lado, el contenido de proteína NF-κB del músculo esquelético en los grupos D0, D24 y D48, así como en el grupo E48, se vio notablemente regulado a la baja (P <0,05), y el del grupo E48 también se vio notablemente regulado a la baja (P <0,05). Conclusión NF-κB puede regular negativamente el proceso de degradación de la proteína a través de la vía NF-κB / MuRF1. Nivel de evidencia III; Estudios terapéuticos que investigan los resultados del tratamiento.

RESUMO Objetivo Estudar os efeitos do trauma contuso e do exercício exaustivo na expressão dos fatores relacionados à degradação MuRF1 e MAFbx no músculo esquelético de ratos e descrever o mecanismo de reparo da lesão muscular esquelética. Métodos Quarenta e dois ratos SD machos foram divididos aleatoriamente em 7 grupos. Os ratos de cada grupo foram mortos em diferentes momentos (0h, 24h, 48h) após exercício exaustivo (E0, E24, E48) e trauma contuso (D0, D24, D48), respectivamente, e no estado de repouso no grupo controle (C). Os músculos gastrocnêmios direitos foram ressecados e divididos em duas partes, uma para os mRNAs de MuRF1 e MAFbx por PCR em tempo real e outra para a medição de proteínas a partir do Western blot. Resultados Em comparação com o grupo controle, o mRNA de MuRF1 e a expressão proteica do músculo esquelético no grupo E0 foram acentuadamente aumentados (P <0,05) e seguidos por uma tendência descendente nos grupos E24 e E48. Por outro lado, a expressão do mRNA de MuRF1 do músculo esquelético no grupo D24 foi significativamente regulada para cima (P <0,01), depois diminuiu no grupo D48 (P <0,01). Enquanto isso, em comparação com o grupo C, a expressão gênica do mRNA de MAFbx continuou regulada para cima em D24 e D48 (P <0,05), mas diminuiu em E24 e E48 (p<0,01). Por outro lado, os teores de proteína NF-κB do músculo esquelético nos grupos D0, D24 e D48, bem como no grupo E48, foram marcadamente regulados para baixo (P <0,05), e o do grupo E48 também foi notavelmente regulado para baixo (P <0,05). Conclusão NF-κB pode regular negativamente o processo de degradação da proteína pela via NF-κB / MuRF1. Nível de evidência III; Estudos terapêuticos que investigam os resultados do tratamento.

Comparative study of the Rheum tanguticum's chemical contents based on spatial distribution characteristics.

Rheum tanguticum (R. tanguticum) has been widely used for the treatment of inflammatory diseases in clinical. However, limited research exist on the quality evaluation of various R. tanguticum locations, which has certain drawbacks. In this study, Fourier-transform infrared spectroscopy (FTIR) and high-performance liquid chromatography (HPLC) were used to comparative study on the chemical contents of R. tanguticum, to clarify the relationship between the chemical contents and the spatial distribution of R. tanguticum. First of all, the FTIR spectra of 18 batches of R. tanguticum were examined. Following the cluster analysis, the FTIR spectra of various production locations differed. To some extent, establishing the double index analysis sequence of common and variation peaks may differentiate distinct production locations of medicinal materials. The HPLC fingerprint of R. tanguticum was constructed to further explore the link between components and their origin. PCA of common peaks of 18 batches of R. tanguticum indicated that R. tanguticum grown in Gannan and Qinghai had a tendency to separate t[2], however this trend was not noticeable. Then, OPLS-DA model was established, and the key differential components of R. tanguticum produced in Gannan and Qinghai were discovered to be R16, R37, R46, and R47 (Aloe emodin) (VIP ≥ 1 and P < 0.05). At last, Pearson's test was used to examine the relationship between longitude, latitude, altitude, and composition. Longitude was significantly positively correlated with R28 and R30 (P < 0.05), and a very significantly positively correlated with R35, R36, R37, R46, and R47 (P < 0.01). Latitude was significantly negatively correlated with R34, R35, and R40 (P < 0.05), and extremely significantly negatively correlated with R28, R30, R36, R37, R46, and R47 (P < 0.01). Altitude was significantly positive correlation with R36 and R37 (P < 0.01). The results of our study can provide insights into R. tanguticum quality control and aid in establishing a natural medication traceability system.

The Function of Natural Polysaccharides in the Treatment of Ulcerative Colitis.

Ulcerative colitis (UC) is an inflammatory bowel disease that is persistent and nonspecific. There are several medications available for the treatment of UC. However, conventional UC medications have substantial adverse effects, low clinical effectiveness, and a high recurrence rate. Therefore, it is critical to discover new medicines that are both safe and effective for UC patients. Natural polysaccharides offer a wide range of pharmacological benefits, including anti-inflammatory, anti-virus, anti-tumor, anti-aging, immune enhancement, and gut flora regulation. In the therapy of UC, natural polysaccharides can modulate inflammatory factors, the immune system, and intestinal flora, and preserve the intestinal mucosa. It demonstrates a good curative effect and is of safety to use, thereby being a potential treatment for UC patients. This paper covers the structure, the pharmacological effects on UC, and the mechanisms of natural polysaccharides. Finally, limitations, challenges, and perspectives are discussed. It is hoped that the findings of this publication will inspire more natural polysaccharides research and provide a theoretical foundation for the creation of new UC medications.

Mechanism of Porphyromonas gingivalis-lipopolysaccharide in regulating the insulin signaling pathway in adipocytes via X-box binding protein 1.

OBJECTIVES: This study aims to investigate the effect of X-box binding protein 1 (XBP1), a key signal molecule of ERS, on the insulin signaling pathway in adipocytes stimulated by Porphyromonas gingivalis (P. gingivalis)-lipopolysaccharide (LPS), a pathogenic bacterium of periodontitis. METHODS: Primary cultured rat adipocytes were stimulated by P. gingivalis-LPS (100 ng·mL-1) for 4, 8, 12, and 24 h. The protein expression levels of insulin receptor substrate-1 (IRS-1), phosphoinositide dependent protein kinase (p-PDK-1), and protein kinase B (p-AKT-1) in the insulin signaling pathway were detected by Western blot analysis. pLVX-NC1, pLVX-XBP1, pLVX-NC2, and pLVX-XBP1-RNAi were transfected into adipocytes, respectively. The transfected rat adipocytes were stimulated by P. gingivalis-LPS, and the protein expression of the insulin signaling pathway was detected by Western blot. RESULTS: The Western Blot showed decreased protein expression of the insulin signaling pathway in rat adipocytes stimulated with P. gingivalis-LPS compared with the control, and the difference was statistically significant (P<0.05). The protein expression levels of IRS-1, p-PDK-1, and p-AKT in the rat adipocytes of pLVX-XBP1 were significantly higher than those in pLVX-NC1 at 8 and 12 h after P. gingivalis-LPS stimulation (P<0.05). The protein expression levels of IRS-1, p-PDK-1, and p-AKT in the rat adipocytes of pLVX-XBP1-RNAi were significantly lower than those in pLVX-NC2 at 4, 8, 12, and 24 h after P. gingivalis-LPS stimulation (P<0.05). CONCLUSIONS: P. gingivalis-LPS regulates the insulin signaling pathway in adipocytes th-rough XBP1.

Effects of contusion and exhaustive exercise on mg53, ptrf in skeletal muscle of rats / Efeitos da contusão e do exercício exaustivo sobre mg53, ptrf em músculos esqueléticos de ratos / Efectos de la contusión y del ejercicio exhaustivo sobre mg53, ptrf en músculos esqueléticos en ratones

ABSTRACT Objectives To study the effects of contusion and exhaustive exercise on gene expression of MG53, PTRF, Pax7 and β-catenin in skeletal muscle of rats, and reveal the repair mechanism of skeletal muscle injury. Methods Forty-two male Wistar rats were randomly divided into 7 groups, with 6 rats in each group. All groups were euthanized at different time points after exhaustive exercise and contusion, respectively, while the control group was euthanized in resting state. The right gastrocnemius muscles were measured for mRNAs of MG53, PTRF, Pax7 and β-catenin by real time PCR. Results MG53 mRNA and PTRF mRNA of skeletal muscle in groups immediately after exhaustive exercise and after contusion increased significantly (p<0.05), while the two indices decreased constantly at 24 and 48 hours after injury with a similar change trend. Compared with the control group, Pax7 mRNA of skeletal muscle as a marker showed no significant difference in exhaustive exercise groups, but decreased at 48 hours after contusion (p<0.05). β-catenin mRNA of skeletal muscle down-regulated significantly over 24 hours after injury, then activated with an increased value at 48 hours after contusion (p<0.05). As a whole, the variations in the above indices in the contusion groups covered a wider range than in the exhaustive exercise groups. Conclusion The cytomembrane repair mechanism of MG53 and PTRF began immediately after the end of exhaustive exercise and contusion. Activation of Pax7 as the satellite cell marker took longer, and Wnt/β-catenin pathway showed first a decrease and then an increase resulting from the time-dependent gene expression during the repair of skeletal muscle injury. Level of evidence III, Therapeutic studies investigating the results of treatment.

RESUMO Objetivos Estudar os efeitos da contusão e do exercício exaustivo sobre a expressão de MG53, PTRF, Pax7 e β-catenina no músculo esquelético de ratos e revelar o mecanismo de reparo da lesão desses músculos. Métodos Quarenta e dois ratos Wistar machos foram divididos randomicamente em 7 grupos, com 6 ratos em cada grupo. Todos os grupos foram sacrificados em diferentes momentos após exercícios exaustivos e contusão, respectivamente, enquanto o grupo controle foi sacrificado em repouso. O músculo gastrocnêmio direito de todos os ratos foi analisado por PCR em tempo real, quanto ao RNAm de MG53, PTRF, Pax7 e β-catenina. Resultados O RNAm de MG53 e de PTRF no músculo esquelético dos grupos imediatamente após o exercício exaustivo e após a contusão aumentou significativamente (p < 0,05), enquanto a diminuição foi constante 24 e 48 horas depois da lesão, com tendência de mudança semelhante. Comparado com o grupo controle, o RNAm de Pax7 do músculo esquelético não mostrou diferença significativa como marcador nos grupos de exercício exaustivo, mas diminuiu 48 horas depois da contusão (p < 0,05). O RNAm da β-catenina do músculo esquelético diminuiu significativamente ao longo de 24 horas após a lesão e, a seguir, voltou para um valor elevado 48 horas depois da contusão (p < 0,05). Como um todo, as variações nos grupos de contusão tiveram uma faixa mais ampla do que a dos grupos de exercícios exaustivos. Conclusões O mecanismo de reparação da citomembrana de MG53 e PTRF começou imediatamente depois do término de exercício exaustivo e contusão. A ativação do Pax7 como marcador das células satélite demorou mais tempo e a via Wnt/β-catenina mostrou primeiro diminuição e depois aumento decorrente da expressão gênica dependente do tempo durante o reparo da lesão muscular esquelética. Nível de Evidência III, Estudos Terapêuticos - Investigação de resultados do tratamento.

RESUMEN Objetivos Estudiar los efectos de la contusión y del ejercicio exhaustivo sobre la expresión de MG53, PTRF, Pax7 y β-catenina en el músculo esquelético de ratones y revelar el mecanismo de reparación de la lesión de esos músculos. Métodos Cuarenta y dos ratones Wistar machos fueron divididos aleatoriamente en 7 grupos, con 6 ratones en cada grupo. Todos los grupos fueron sacrificados en diferentes momentos después de ejercicios exhaustivos y contusión, respectivamente, mientras que el grupo control fue sacrificado en reposo. El músculo gastrocnemio derecho de todos los ratones fue analizado por PCR en tiempo real, cuanto al RNAm de MG53, PTRF, Pax7 y β-catenina. Resultados El RNAm de MG53 y de PTRF en el músculo esquelético de los grupos inmediatamente después del ejercicio exhaustivo y después de la contusión aumentó significativamente (p < 0,05), mientras que la disminución fue constante 24 y 48 horas después de la lesión, con tendencia de cambio semejante. Comparado con el grupo control, el RNAm de Pax7 del músculo esquelético no mostró diferencia significativa como marcador en los grupos de ejercicio exhaustivo, pero disminuyó 48 horas después de la contusión (p < 0,05). El RNAm de la β-catenina del músculo esquelético disminuyó significativamente a lo largo de 24 horas después de la lesión y, a continuación, volvió para un valor elevado 48 horas después de la contusión (p < 0,05). Como un todo, las variaciones en los grupos de contusión tuvieron una franja más amplia que la de los grupos de ejercicios exhaustivos. Conclusiones El mecanismo de reparación de la citomembrana de MG53 y PTRF comenzó inmediatamente después del término de ejercicio exhaustivo y contusión. La activación del Pax7 como marcador de las células satélite demoró más tiempo y la vía Wnt/β-catenina mostró primero disminución y después aumento proveniente de la expresión génica dependiente del tiempo durante la reparación de la lesión muscular esquelética. Nivel de Evidencia III, Estudios Terapéuticos - Investigación de resultados del tratamiento.