Acute liver failure (ALF) is a life-threatening disease characterized by the rapid development of hepatocyte death and a systemic inflammatory response, which leads to high mortality. Despite the prevention of ALF complications, therapeutic effectiveness remains limited because of the rapid disease progression. Thus, there is a need to explore various therapeutic approaches. Currently, the only effective treatment is liver transplantation; However, the lack of donors, surgical complications, immunosuppression, and high medical costs limit its clinical application. Recently, mesenchymal stem cells (MSCs) have been found to exert hepatoprotective effects in ALF through suppression of inflammation, immunoregulation, promotion of mitosis, anti-apoptosis effects, and alleviation of the metabolic and oxidative stress imbalance. In this review, we summarize the advantages and disadvantages of MSCs from different sources and their molecular mechanisms in ALF treatment, along with future perspectives that may provide guidance to improve the current status of MSCs therapy for ALF.

Objective:To investigate the role of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) in regulating proliferation of airway smooth muscle cells in ovalbumin(OVA)-induced asthma rats. Methods：Male Wistar rats (n=16) were randomized into OVA-induced asthma group and control group(8 rats each). The histomorphological changes of bronchia and lung tissues were observed by H-E staining. The expressions of proliferating cell nuclear antigen(PCNA) and PTEN were assayed by immunohistochemistry. Reverse transcription-polymerase chain reaction(RT-PCR) was carried out to determine the changes in the expression of PTEN mRNA. Results: The typical pathological features of asthma were revealed in the OVA-exposed rats including numerous inflammatory cells infiltrated around the bronchia and in the lung tissues, the thickened airway smooth muscle and the narrowed airway. The levels of PCNA were distinctly increased in OVA-induced asthma group than that of control（P < 0.05），while the levels of PTEN and PTEN mRNA were significantly decreased in lung tissues of OVA-exposed rats（P < 0.05）. Conclusion：The gene inactivation of PTEN may play a pivotal role in proliferation of airway smooth muscle cells in asthma rats, and the most probable mechanism is associated with the functions of PI3K signaling pathway.