Obese sarcopenia is a progressive loss of skeletal muscle mass and strength with increases in adipocytes. The aim of this study was to investigate the effects of combination of exercise training and resveratrol on the pathological pathway from obesity to sarcopenia, and potential therapy for skeletal muscle declines in physical function. Two animal models were experimented: (1) C57BL/6J male mice were fed either a high-fat diet (HFD) for 8 weeks to induce obesity and resveratrol (low-, middle-, and high-dose) for 4 weeks. (2) senescence-accelerated mouse prone 8 (SAMP8) mice with sarcopenia were used. Skeletal muscle function of SAMP8 mice expressed an age-associated decline. In SAMP8 mice, resveratrol (150 mg/Kg BW, daily) was administered by oral gavage two times a week for 1 month of the experimental period. Exercise training based on adaptations in the muscle is training twice a week for 4 weeks. SAMP8 mouse skeletal muscle in each group was analyzed by H and E staining, transferase dUTP nick end labeling, and Western blot analysis. Mitochondrial function expression, apoptosis and relative hypertrophy signaling in HFD-induced obesity mice and SAMP8 mice were determined by Western blot analysis. Results of the present study indicate that effect of resveratrol on skeletal muscles of HFD-induced obesity mice is linked to an increase in Bcl-2 and phosphatidylinositol 3 kinase/AKT expressions. On the other hand, resveratrol, and its combination with exercise training, attenuate the aging-related mitochondrial dysfunction involving Bad, caspase 3, and interleukin-6 expressions in SAMP8 mice. Combination of exercise training and resveratrol induced hypertrophy in skeletal muscles of sarcopenia SAMP8 mice. Therefore, we suggest combination of exercise training and resveratrol as a therapeutic potential in obese sarcopenia.

The aim of this study was to establish the effective hepatoprotective properties of traditional Chinese medicines (TCMs) in fibrotic rat liver regeneration after partial hepatectomy (PHx). Fibrosis was induced in rats by ethanol (EtOH, 5 ml/kg) administration for 6, 24, 72, and 168 h. The rats were then fed four TCMs (1 g/kg/day, Codonopsis pilosula (CP), Salvia miltorrhiza Bunge (SMB), Bupleurum kasi (BK), and Elephantopus scaber L (ESL)) to Spraque-Dawley rats for 6, 24, 72, and 168 h, respectively. Surgical 70% cirrhotic fibrosis PHx was then conducted at 6, 24, 72, and 168 h. The effects on liver regeneration were examined to estimate and measure hepatocyte growth factor (HGF), focal adhesion kinase (FAK), Cyclin D1, Cyclin E, and retinoblastoma protein (pRb) protein expression using Western blotting analysis. Cyclin D1, matrix metalloproteinase (MMP)-2, MMP-9, tissue inhibitors of metalloproteinase (TIMP)-1, TIMP-2 and TIMP-3 mRNA by Reverse transcription polymerase chain reaction (RT-PCR) were analyzed in cirrhotic fibrosis rats. transforming growth factor-β1 (TGF-β1), Cyclin D1, Cyclin E, pRb and E2F mRNA expression levels were determined in fibrotic rats following PHx using RT-PCR. We found elevated glutamyl oxaloacetic transaminase (GOT), glutamyl pyrubic transaminase (GPT), alkaline phosphatase (ALP), gammaglutamyl transpeptidase (γ-GT), glutathione (GSH) and nonprotein sulfhydryl (NPSH) and total bilirubin in serum after 6 h EtOH administration. These levels were progressively decreased over 168 h. Total protein and albumin were reduced in serum Subcutaneafter 6 h administration and then progressively increased. In contrast, tissues disorder histology and morphology were determined in liver sections. After rats were fed TCMs we found that SMB extraction not only induced HGF, FAK, Cyclin D1, and pRb protein expression and Cyclin D1 mRNA increases, but also reduced MMP-2 and MMP-9 after 24 and 72 h post injury. In the cell cycle S phase the Cyclin E protein expression was increased by ESL. CP induced TIMP-1, TIMP-2 and TIMP-3 mRNA increases in fibrotic rats. We detected liver regeneration in fibrotic rats. We also found that the liver regeneration index increased from 6 to 168 h post PHx. After 168 h fibrotic liver regeneration rats exhibited reduced TGF-β1 mRNA expression and enhanced Cyclin D1, Cyclin E, pRb and E2F mRNA expression. TCMs play a crucial role in the early mediating process in fibrotic rat liver regeneration after PHx.

Background: Little is known about the pathogenesis of cardiomyocyte hypertrophy caused by periodontitis pathogens. The purpose of this study was to determine the effect of the periodontal pathogen Porphyromonas gingivalis on cardiomyocyte hypertrophy.Methods: Matrix metalloproteinase (MMP)‐2 and MMP‐9 activities and cellular morphology were measured by gelatin zymography and immunofluorescence after P. gingivalis‐medium treatment with or without SB203580 (p38 mitogen‐activated protein kinase cascade [p38] inhibitor), U0126 (mitogen‐activated protein kinase kinase [MAPKK] inhibitor), LY294002 (phosphoinositide 3‐kinase [PI3K] inhibitor), cyclosporin A (CsA; calcineurin inhibitor), SP600125 (c‐Jun N‐terminal kinase [JNK] inhibitor), proinflammatory interleukin (IL)‐1, or anti‐inflammatory IL‐10 in cultured cardiomyoblast H9c2 cells.Results: P. gingivalis medium increased MMP‐9 activities and cellular sizes (+87%) of H9c2 cells, whereas Actinobacillus actinomycetemcomitans medium and Prevotella intermedia medium had no effects. The increased activity of MMP‐9 treated with P. gingivalis medium was not mediated through p38, extracellular‐regulated kinase (ERK), PI3K, calcineurin, and JNK signaling pathways and was not inhibited by IL‐10. However, the hypertrophy of H9c2 cells induced with P. gingivalis medium was reduced by administration of SB203580 (−37%), U0126 (−35%), LY294002 (−49%), CsA (−49%), and SP600125 (−24%).Conclusions: Our findings suggest that P. gingivalis medium elevated MMP‐9 activity and induced cardiomyoblast hypertrophy. However, P. gingivalis‐induced H9c2 cell hypertrophy was mediated through p38, ERK, PI3K, calcineurin, and JNK signaling pathways, which are in a totally different regulatory pathway from P. gingivalis‐elevated MMP‐9 activity. These findings provide evidence that P. gingivalis infection activated multiple factors via different pathways to induce the development of hypertrophy of H9c2 cardiomyoblast cells.

Partial hepatectomy (PHx) is a liver regeneration physiological response induced to maintain homeostasis. Liver regeneration evolved presumably to protect wild animals from catastrophic liver loss caused by toxins or tissue injury. Silymarin (Sm) ability to stimulate liver regeneration has been an object of curiosity for many years. Silymarin has been investigated for use as an antioxidant and anticarcinogen. However, its use as a supportive treatment for liver damage is elusive. In this study, we fed silymarin (Sm, 25 mg/kg) to male Sprague-Dawley rats for 7 weeks. Surgical 2/3 PHx was then conducted on the rats at 6 hrs, 24 hrs, and 72 hrs. Western blot and RT-PCR were conducted to detect the cell cycle activities and silymarin effects on hepatic regeneration. The results showed that silymarin enhanced liver regeneration by accelerating the cell cycle in PHx liver. Silymarin led to increased G1 phase (cyclin D1/pRb), S phase (cyclin E/E2F), G2 phase (cyclin B), and M phase (cyclin A) protein and mRNA at 6 hrs, 24 hrs, and 72 hrs PHx. HGF, TGFα, and TGFβ1 growth factor expressions were also enhanced. We suggest that silymarin plays a crucial role in accelerated liver regeneration after PHx.