Liver diseases pose a serious problem for national health care system all over the world. Liver regeneration has profound impacts on the occurrence and development of various liver diseases, and it remains an extensively studied topic. Although current knowledge has suggested two major mechanisms for liver regeneration, including compensatory hyperplasia of hepatocytes and stem or progenitor cell-mediated regeneration, the complexity of this physiopathological process determines that its effective regulation cannot be achieved by single-target or single-component approaches. Alternatively, using traditional Chinese medicine (TCM) to regulate liver regeneration is an important strategy for prevention and treatment of liver disorder and the related diseases. From the perspectives of TCM, liver regeneration can be caused by the disrupted balance between hepatic damage and regenerative capacity, and the “marrow”-based approaches have important therapeutic implications for liver regeneration. These two points have been massively supported by a number of basic studies and clinical observations during recent decades. TCM has the advantages of overall dynamic fine-tuning and early adjustment, and has exhibited enormous therapeutic benefits for various liver diseases. Here, we review the recent advances in the understanding of liver regeneration in TCM system in the hope of facilitating the application of TCM for liver diseases via regulation of liver regeneration.

Introduction: There is a growing need for chondrocyte implantation for reconstructing cartilage defect. However, ossification of the implanted cartilage is a challenging problem. Implant-type tissue-engineered cartilage from human auricular chondrocytes is a three-dimensional implant type cartilage using PLLA as a scaffold for chondrocytes. Although there is a study which evaluated the ossification of this cartilage in subcutaneous area, there is no study which clarify the possibility of ossification in osteoinductive surroundings. The purpose of this study was to elucidate the possibility of the ossification of implant-type tissue-engineered cartilage using human auricular chondrocyte in an osteoinductive environment. Methods: Human chondrocytes were harvested from ear cartilage. After dispersion by enzyme digestion, they were put into either a poly-L-lactic acid (PLLA) or poly lactic-co-glycolic acid (PLGA) scaffold, with collagen gel. Implant-type tissue-engineered cartilage was interposed between pieces of human iliac bone harvested from the same donor and implanted subcutaneously in nude rats. Scaffold without chondrocytes was used as a control. After 1, 3, and 6 months, ossification and cartilage formation were evaluated by X-ray, hematoxylin-eosin (HE) stain and toluidine blue (TB) stain. Results: There was no ossification of implant-type cartilage using human chondrocytes, even under osteoinductive conditions. HE staining showed that perichondrium formed around the constructs and chondrocytes were observed 6months after the implantation. TB staining showed metachromasia in every sample, with the area of metachromasia increasing over time, suggesting maturation of the cartilage. Conclusions: In conclusion, adjacent iliac bone had no apparent effect on the maturation of cartilage in implant-type tissue-engineered cartilage. Cartilage retention and maturation even in the presence of iliac bone could have been due to a scarcity of mesenchymal stem cells in the bone and surrounding area.

Chronic lung diseases are becoming a leading cause of death worldwide. There are few effective treatments for those patients and less choices to prevent the exacerbation or even reverse the progress of the diseases. Over the past decade, cell-based therapies using stem cells to regenerate lung tissue have experienced a rapid growth in a variety of animal models for distinct lung diseases. This novel approach offers great promise for the treatment of several devastating and incurable lung diseases, including emphysema, idiopathic pulmonary fibrosis, pulmonary hypertension, and the acute respiratory distress syndrome. In this review, we provide a concise summary of the current knowledge on the attributes of endogenous lung epithelial stem/progenitor cells (EpiSPCs), mesenchymal stem cells (MSCs) and endothelial progenitor cells (EPCs) in both animal models and translational studies. We also describe the promise and challenges of tissue bioengineering in lung regenerative medicine. The therapeutic potential of MSCs is further discussed in IPF and chronic obstructive pulmonary diseases (COPD).

BackgroundChronic alcohol ingestion may cause severe biochemical and pathophysiological derangements to skeletal muscle. Unfortunately, these alcohol-induced events may also prime skeletal muscle for worsened, delayed, or possibly incomplete repair following acute injury. As alcoholics may be at increased risk for skeletal muscle injury, our goals were to identify the effects of chronic alcohol ingestion on components of skeletal muscle regeneration. To accomplish this, age- and gender-matched C57Bl/6 mice were provided normal drinking water or water that contained 20% alcohol (v/v) for 18–20 wk. Subgroups of mice were injected with a 1.2% barium chloride (BaCl2) solution into the tibialis anterior (TA) muscle to initiate degeneration and regeneration processes. Body weights and voluntary wheel running distances were recorded during the course of recovery. Muscles were harvested at 2, 7 or 14 days post-injection and assessed for markers of inflammation and oxidant stress, fiber cross-sectional areas, levels of growth and fibrotic factors, and fibrosis.ResultsBody weights of injured, alcohol-fed mice were reduced during the first week of recovery. These mice also ran significantly shorter distances over the two weeks following injury compared to uninjured, alcoholics. Injured TA muscles from alcohol-fed mice had increased TNFα and IL6 gene levels compared to controls 2 days after injury. Total protein oxidant stress and alterations to glutathione homeostasis were also evident at 7 and 14 days after injury. Ciliary neurotrophic factor (CNTF) induction was delayed in injured muscles from alcohol-fed mice which may explain, in part, why fiber cross-sectional area failed to normalize 14 days following injury. Gene levels of TGFβ1 were induced early following injury before normalizing in muscle from alcohol-fed mice compared to controls. However, TGFβ1 protein content was consistently elevated in injured muscle regardless of diet. Fibrosis was increased in injured, muscle from alcohol-fed mice at 7 and 14 days of recovery compared to injured controls.ConclusionsChronic alcohol ingestion appears to delay the normal regenerative response following significant skeletal muscle injury. This is evidenced by reduced cross-sectional areas of regenerated fibers, increased fibrosis, and altered temporal expression of well-described growth and fibrotic factors.