Key result
Hydrogen inhibits vascular smooth muscle cell proliferation and attenuates aortic hypertrophy in preclinical models.
Why the study?
Molecular hydrogen has attracted attention for preventing oxidative stress-related vascular diseases, but its effects on VSMC proliferation, migration, and vascular hypertrophy were not fully evaluated.
Hypothesis-generating for hydrogen in vascular remodeling; clinical translation untested and should not yet change practice.
Molecular hydrogen (H₂) has recently attracted considerable attention for the prevention of oxidative stress-related vascular diseases. The purpose of this study is to evaluate the effects of hydrogen on proliferation and migration of vascular smooth muscle cells (VSMCs) stimulated by angiotensin II (Ang II) in vitro, and on vascular hypertrophy induced by abdominal aortic coarctation (AAC) in vivo. Hydrogen-rich medium (0.6~0.9 ppm) was added 30 min before 10⁻⁷ M Ang II administration, then the proliferation and migration index were determined 24 h after Ang II stimulation. Hydrogen gas (99.999%) was given by intraperitoneal injection at the dose of 1 ml/100 g/day consecutively for one week before AAC and lasted for 6 weeks in vivo. Hydrogen inhibited proliferation and migration of VSMCs with Ang II stimulation in vitro, and improved the vascular hypertrophy induced by AAC in vivo. Treatment with hydrogen reduced Ang II- or AAC-induced oxidative stress, which was reflected by diminishing the induction of reactive oxygen species (ROS) in Ang II-stimulated VSMCs, inhibiting the levels of 3-nitrotyrosine (3-NT) in vascular and serum malondialdehyde (MDA). Hydrogen treatment also blocked Ang II-induced phosphorylation of the extracellular signal-regulated kinase1/2 (ERK1/2), p38 MAPK, c-Jun NH₂-terminal kinase (JNK) and the ezrin/radixin/moesin (ERM) in vitro. Taken together, our studies indicate that hydrogen prevents AAC-induced vascular hypertrophy in vivo, and inhibits Ang II-induced proliferation and migration of VSMCs in vitro possibly by targeting ROS-dependent ERK1/2, p38 MAPK, JNK and ERM signaling. It provides the molecular basis of hydrogen on inhibiting the abnormal proliferation and migration of VSMCs and improving vascular remodeling diseases.
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Yaxing Zhang (2016) studied Oxidative stress-related vascular diseases (vascular hypertrophy). Molecular hydrogen (H₂) was evaluated on Proliferation and migration of vascular smooth muscle cells in vitro, and vascular hypertrophy in vivo. Hydrogen inhibited Ang II-stimulated proliferation and migration of vascular smooth muscle cells in vitro and improved abdominal aortic coarctation-induced vascular hypertrophy in vivo.
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