Hyperbaric Oxygen Therapy (HBOT) And Skin Care.

Hyperbaric Oxygen Therapy for Skin Care
Hyperbaric oxygen therapy (HBOT), in which patients breathe pure oxygen in a pressurised oxygen chamber, has been used for many years to treat conditions such as decompression sickness and carbon monoxide poisoning. Oxygen is a crucial component in skin renewal, photoaging treatment, and complexion improvement. Daily exposure to chronic UV radiation, particularly UV-B, can significantly accelerate the rate of wrinkle formation. UV-B accelerate skin angiogenesis and degrading extracellular matrix components. At the moment, there are medical aesthetic clinics that use high-pressure oxygen therapy on the skin to make wrinkles less noticeable.
Utilization of oxygen for rejuvenation
HBOT as a therapy for cosmetic purposes is a relatively new use in UK, have not been a significant number of studies on the use of oxygen therapy for wrinkle removal. It is believed that receiving regular HBOT treatments will increase skin elasticity and stimulate collagen formation. It resulted in a reduction in wrinkles and fine lines and an improvement in skin texture. Numerous dermatology clinics and even spas have employed oxygen-delivering equipment to treat age-related skin conditions. Oxygen is employed in skin care because it is believed that oxygen delivery boosts cell metabolism. The use of oxygen therapy as a method of skin rejuvenation is becoming more prevalent in skin care clinics. However, scientific data is needed to support these statements.
Mechanisms of skin rejuvenation by HBOT
HIF-1α
UV-B radiation can induce angiogenesis by activating the HIF-1 protein, resulting in skin wrinkling. and are the two components of the HIF-1 protein. HIF-1 is the subunit that is directly associated with hypoxia-induced responses. HIF-1 mRNA is regularly synthesised in cells. During hypoxia, the mRNA level of HIF-1 rises in some cells, leading to an increase in the transcription of numerous genes, including VEGF. However, mRNA level remains unchanged while the HIF-1 protein level rises, showing that under normal oxygen levels, the HIF-1 protein is typically degraded by proteasomes. Lower oxygen tension stabilises the HIF-1 subunit and stimulates angiogenesis to compensate for hypoxia.
Since HIF-1 subunits are destroyed under normal oxygen levels, this suggests that raising oxygen tension in the epidermal cells via oxygen therapy could promote proteasomal degradation of HIF-1 subunits, hence reducing angiogenesis and slowing skin wrinkling. This study demonstrates that an increase in oxygen level leads to an increase in HIF-1 protein degradation and shows that an increase in oxygen tension can reduce wrinkle formation due to a decrease in angiogenesis.
Even while the level of VEGF, which is a downstream of the HIF-1 protein, was shown to be elevated in both the UVB and UVB + HBO groups, the UVB + HBO group showed a decreased tendency to increase. So, it’s possible that hyperbaric chamber slows the formation of wrinkles by stopping the HIF-1 angiogenesis-signaling pathway.
MMP-2 & MMP-9
MMP stands for matrix metalloproteinases, which are zinc-dependent proteins involved in extracellular matrix remodelling and play important roles in angiogenesis, morphogenesis, and metastasis.The protein consists of many domains, including propeptide, catalytic, and hemopexin domains. MMPs participate in the degradation of collagen, proteoglycans, and many glycoproteins.
MMPs are secreted as inactive zymogens (pro-MMP) and must be activated to reach their full functional potential. Typically, growth factors and cytokines influence the activation or inhibition of pro-MMP production at the transcriptional level. MMP-1, 2, 3, and 9 are the photoaging-related MMPs whose levels increased in trials with human fibroblasts following UV exposure. In other investigations conducted on MMPs in the epidermis of hairless mouse skin, UV-irradiation did not significantly raise the levels of MMP-1 and MMP-3.
Gelatinase A and gelatinase B
Commonly known as gelatinase A and gelatinase B, they are primarily responsible for digesting type IV and type VII collagens, which are essential components of the basement membrane. When CGS27023A, a potent synthetic inhibitor of MMP-2 and MMP-9, was applied topically over a period of time, significant inhibition of the reduction of collagen by UVB radiation was observed.
Even though MMP-2 and MMP-9 play critical roles in producing skin wrinkling and angiogenesis. MMP-9 levels were found to be the same in both the UVB and UVB + HO groups, but MMP-2 levels were found to be somewhat lower in both groups. Since MMP-2 levels were reduced in both the UVB and UVB + HO groups, it remains to be determined if hyperoxic conditions affect MMP-2 levels. If you want a better result, you may need to change the amount of oxygen or how long you do HBOT for.
Cellular infiltration due to inflammation
Inflammatory cells, particularly neutrophils, are capable of causing damage to the extracellular matrix and have destructive potential. The tissue-destructive actions of neutrophils are responsible for emphysema, adult respiratory distress syndrome, adult periodontitis, rheumatoid arthritis, ulcerative colitis, and blistering skin illnesses. Neutrophils are the most numerous white blood cells, and at a certain threshold of tissue injury, they rapidly leave the bloodstream and travel to the site of the damage.
Exposure to sunshine and an erythemogenic, or erythema-causing, dose of UVB radiation can result in an influx of neutrophils that produce solar elastosis, or the breakdown and loss of elastic tissue. Neutrophils are packed with potent proteolytic enzymes capable of dissolving collagen and elastic fibres, thereby causing damage to the extracellular matrix, which contributes to their destructive capabilities.
Neutrophils are capable of releasing a group of serine proteases, most notably the proteolytic neutrophil elastase. Due to the fact that more research has focused on the hypothesis that MMPs and HIF1 are the primary causes of wrinkles. The rate of neutrophil infiltration can only be measured in skin that has recently been exposed to UV radiation, neutrophils have not received a great deal of attention for their role in causing wrinkles.
UVB-irradiation can produce angiogenesis in the skin, and these new blood vessels may be the primary source of the increase in inflammatory cell infiltration that leads to wrinkle formation. Oxygen recovery chamber may be useful for the treatment of skin wrinkles since it may reduce the quantity of inflammatory cell infiltration and neutrophil releasing MMPs.
Reducing blood flow in active muscle cells
It was discovered and demonstrated that hyperoxic circumstances can reduce blood flow in active muscle cells and impede active angiogenesis in the skin. Hyperbaric therapy can decrease skin angiogenesis by boosting the degradation of the HIF1 protein. With this angiogenesis pathway suppressed, new blood vessels are not produced, which reduces the number of infiltrating neutrophils and reduces the production of MMPs in the skin. Recent research reveals, however, that hyperbaric therapy circumstances could not have simply altered HIF1 degradation and reduced wrinkle formation.
It was shown that suppression of HIF1 protein alone was insufficient to prevent the creation of wrinkles in response to a higher dosage of UV radiation, which led to the regulation of MMP activity. Additional research is required to determine the particular conditions and mechanism by which hyperbaric environments inhibit the production of skin wrinkles.
Thrombospondin-1
Thrombospondin-1 (TSP-1) is a matricellular protein that inhibits the proliferation and migration of endothelial cells but more significantly, in this instance, substantially reduces angiogenesis. The human basal epidermal keratinocyte produces its own mRNA, and the TSP-1 protein is deposited in the basement membrane region. Recent research indicates that TSP-1’s capacity to reduce skin wrinkles stems not only from its ability to prevent angiogenesis but also from its ability to block activation of MMP-2 and MMP-9.
In addition to dissolving the basement membrane and altering the extracellular matrix, activation of MMP-2 is related to increased blood vessel formation, whereas inhibition of this protein decreases the level of angiogenesis. TSP-1 interacts with MMP-2 by attaching to it, inhibiting MMP-2’s action. It is also believed that MMP-9 can accelerate wrinkle formation, hence its interaction with TSP-1 is being investigated. TSP-1 interacts with and inhibits the activity of MMP-9 by binding to it similarly to how it attaches to MMP-2 because MMP-2 and MMP-9 have structurally similar domains.
TSP-1’s capacity to inhibit MMPs contributes to both its anti-angiogenic actions and its ability to diminish UVB-induced skin damage and wrinkles. Although TSP-1 has inhibitory actions that can inhibit angiogenesis and slow the creation of wrinkles, and hyperoxia conditions and therapies have inhibitory activity on angiogenesis. MMP levels, a direct connection between TSP-1 activity and hyperoxia state has not been established. Apparently, additional research is required to determine whether high oxygen tension can enhance the amount of TSP-1, thereby reducing skin wrinkles.
Conclusion
Since its initial usage to treat decompression sickness, the medical application of hyperbaric oxygen therapy has come a long way. HBOT has a lot of potential for skin care, but it needs to be studied more to find out exactly how it stops wrinkles from forming and slows down photoaging.