There is growing evidence that mesenchymal stem cell-derived extracellular vesicles and exosomes can significantly improve the curative effect of oxidative stress-related diseases. Mesenchymal stem cell extracellular vesicles and exosomes (MSC-EVs and MSC-Exos) are rich in bioactive molecules and have many biological regulatory functions. In this review, we describe how MSC-EVs and MSC-Exos reduce the related markers of oxidative stress and inflammation in various systemic diseases, and the molecular mechanism of MSC-EVs and MSC-Exos in treating apoptosis and vascular injury induced by oxidative stress. The results of a large number of experimental studies have shown that both local and systemic administration can effectively inhibit the oxidative stress response in diseases and promote the survival and regeneration of damaged parenchymal cells. The mRNA and miRNAs in MSC-EVs and MSC-Exos are the most important bioactive molecules in disease treatment, which can inhibit the apoptosis, necrosis and oxidative stress of lung, heart, kidney, liver, bone, skin and other cells, and promote their survive and regenerate.

Oxidative stress is defined as an injury resulting from a disturbance in the dynamic equilibrium of the redox environment due to the overproduction of active/radical oxygen exceeding the antioxidative ability of the body. This is a key step in the development of various diseases. Oxidative stress is modulated by different factors and events, including the modification of histones, which are the cores of nucleosomes. Histone modification includes acetylation and deacetylation of certain amino acid residues; this process is catalyzed by different enzymes. Histone deacetylase 6 (HDAC6) is a unique deacetylating protease that also catalyzes the deacetylation of different nonhistone substrates to regulate various physiologic processes. The intimate relationship between HDAC6 and oxidative stress has been demonstrated by different studies. The present paper aims to summarize the data obtained from a mechanistic study of HDAC6 and oxidative stress to guide further investigations on mechanistic characterization and drug development.

Oxidative stress is defined as injury resulting from the disturbance on dynamic equilibrium of redox environment due to over-production of active/ radical oxygen exceeding the anti-oxidative ability in the body. It is a key step of genesis and development of various diseases. Oxidative stress is modulated by different factors and events, including modification of histone, the core of nucleosome. Modification of histone includes acetylation and deacetylation on certain amino acid residues; the process is catalyzed by different enzymes. Histone deacetylase 6 (HDAC6) is a unique deaetylating protease; it also catalyzes deacetylation of different non-histone substrates so as to regulate various physiologic processes. The intimate relationship between HDAC6 and oxidative stress has been demonstrated by different lines of study. The present paper aims at summarizing the data obtained from mechanistic study between HDAC6 and oxidative stress, in order to provide guidance for further investigations in term of mechanistic characterization and drug development.

Oxidative stress is defined as injury resulting from the disturbance on dynamic equilibrium of redox environment due to over-production of active/ radical oxygen exceeding the anti-oxidative ability in the body. It is a key step of genesis and development of various diseases. Oxidative stress is modulated by different factors and events, including modification of histone, the core of nucleosome. Modification of histone includes acetylation and deacetylation on certain amino acid residues; the process is catalyzed by different enzymes. Histone deacetylase 6 (HDAC6) is a unique deaetylating protease; it also catalyzes deacetylation of different non-histone substrates so as to regulate various physiologic processes. The intimate relationship between HDAC6 and oxidative stress has been demonstrated by different lines of study. The present paper aims at summarizing the data obtained from mechanistic study between HDAC6 and oxidative stress, in order to provide guidance for further investigations in term of mechanistic characterization and drug development.

Background Wound healing is a common clinical pathological process that is interrupted when abnormal pathological factors are present, which can significantly delay wound healing and lead to complication. Epigenetic modification plays an important role in wound repair, including histone deacetylase HDAC6-mediated regulation of cell morphology, autophagy, migration, inflammation, and oxidative stress.Therefore, this study aimed to investigate how HDAC6 inhibitors affect the proliferation and migration of dermal fibroblasts in allogeneic skin wound repair. Methods and results We effectively isolated primary skin fibroblasts from newborn rat skin tissue, and the effects of TGFB1 and different concentrations of HDAC6 inhibitor Tubacin on skin fibroblast growth and migration were detected using the MTT assay and scratch test. Tubacin was discovered to decrease fibroblast growth and migration. Tubacin down-regulated the expression levels of COL3, p-AKT, HDAC6, Col1a1, -SMA, and p-ERK, which were up-regulated by TGF-1, in fibroblasts treated with TGF-1 and different doses of Tubacin. Tubacin also increased the protein levels of ace–tubulin and CD31 (platelet endothelial cell adhesion molecule). To examine the impact of the HDAC6 inhibitor Tubacin in skin wound regeneration, we created a full-thickness wound model on the back of rats and used Western blot to assess the expression levels of HDAC6, acetylated -tubulin, COL1A1, COL3, and -SMA. The results demonstrated that trauma increased the expression levels of HDAC6 and acetylated -tubulin in the skin; these findings suggest that HDAC6 and acetylated -tubulin may be involved in wound repair. Tubacin, on the other hand, decreased the protein levels of HDAC6 and acetylated-tubulin, as well as the protein levels of COL1A1 and COL3. The mechanism could be that COL1A1, COL3, and -SMA expression, which are involved in pathological wound repair, are blocked via modulating the TGF-β-PI3K-Akt pathway and MAPK/ERK signaling.Thus, our results implies that inhibiting HDAC6 plays a beneficial function in wound healing and scar formation. Conclusion Tubacin inhibits fibroblast proliferation and migration, as well as the expression of COL1A1, COL3, and -SMA, all of which are involved in pathological wound repair. It also promotes the expression of CD31, which is associated with inflammation or angiogenesis, by regulating the tgf-PI3K-Akt pathway and the MAPK/ERK signaling pathway.