Италийн University of Rome Foro Italico-ийн судлаачид эдгээр эмийн бодис нь булчингийн эсүүдийн нөхөн төлжих чадварыг сайжруулдаг болохыг Molecular Biology Reports сэтгүүлд нийтэлсэн судалгаагаар илрүүлсэн байна.
Одоогийн байдлаар бэлгийн сулрал болон уушгины артерийн даралт ихсэх өвчнийг эмчлэхэд ашигладаг тадалафил эм нь хулганы булчингийн урьдал эсүүдэд нөлөөлж, эсийн үхлийг бууруулж, нөхөн төлжилтийг идэвхжүүлж байгааг лабораторийн туршилтаар тогтоожээ. Булчингийн эд эсийн нөхөн төлжилтийг зохицуулдаг азотын исэл болон cGMP молекулын үйл ажиллагааг тадалафил нь PDE5 ферментийг блоклох замаар уртасгадаг болохыг судалгааны баг тайлбарлаж байна. Энэхүү үйлчилгээ нь шархны эдгэрэлтийг хурдасгаж, булчингийн үүдэл эсийн нөөцийг нэмэгдүүлдэг болох нь туршилтаар батлагджээ.
Тус судалгаанд оролцсон эсүүд тадалафилийн нөлөөгөөр булчингийн ширхэг болон хувирах явц нь түр зуур хойшилж байгаа нь ажиглагдсан бөгөөд үүнийг судлаачид булчингийн үүдэл эсийн нөөцийг нэмэгдүүлэх ач холбогдолтой гэж үзэж байна. Цаашид энэхүү үр дүн нь хүнд хэлбэрийн булчингийн хатингаршилтай өвчтөнүүдэд эмчилгээний шинэ боломж нээж магадгүй ч хүний бие махбодод үзүүлэх нөлөөллийг тогтоохын тулд нэмэлт судалгаа шаардлагатай юм.
Мөн уг бодис нь тамирчдын булчингийн үйл ажиллагааг сайжруулах зорилгоор буруугаар ашиглагдаж болзошгүй тул допингийн эсрэг байгууллагууд үүнийг анхааралдаа авах шаардлагатай гэж судлаачид анхааруулжээ. Тадалафил нь булчингийн нөхөн төлжилтийг дэмжих хүчирхэг нөлөөтэй тул ирээдүйд булчингийн өвчлөлийг эмчлэхэд туслах эмчилгээний нэмэлт хэрэгсэл болох боломжтойг судалгааны баг онцолсон байна.
Дэлгэрэнгүйг эх сурвалжаас харах
↓Эх сурвалжийг нээх ↓
Regular exercise is one of the best ways to stay fit and healthy, but many of us lack the time or motivation to stick to a workout schedule. For some, chronic conditions and disabilities make exercise difficult or impossible.
With that in mind, scientists have long been looking for drugs that could replicate some of the benefits of exercise, without the actual sweat and movement.
Researchers from the University of Rome Foro Italico have now published a study in Molecular Biology Reports reporting that the medication tadalafil, currently prescribed for erectile dysfunction and pulmonary arterial hypertension, could also boost tissue regeneration and repair in muscles.
Using mouse muscle precursor cells in the lab, the researchers found that doses of tadalafil increased the number of cells ready to be transformed into muscle and reduced the number of dead cells.
Essentially, it checks some significant boxes for boosting the regenerative capacity of these cells.
“Prolonged tadalafil treatment significantly increased cell proliferation and survival, reducing cell death at all time points,” write the researchers in their published paper.
Muscle regeneration relies on a particular kind of stem cell, ready and waiting to turn into muscle (a process known as differentiation). This process makes the muscle fibers that can be used for growth and repair.
What we knew coming into this study was that the body uses nitric oxide to trigger muscle regeneration – it’s the signal that gets sent when we exercise or get a muscle injury, and it works via a molecule called cyclic guanosine monophosphate (cGMP).
Muscles shouldn’t regenerate indefinitely, though: an enzyme called phosphodiesterase type 5 (PDE5) keeps cGMP in check, effectively turning it off when the job is done.
That short biology lesson brings us back to this study. We also know tadalafil blocks PDE5, which in theory means cGMP carries on working for longer, without the normal restrictions. That’s what the researchers were testing here.
As well as boosting the number of muscle precursor cells, the tadalafil treatment did something else. When a scratch was put through the cells, it closed up faster with the application of the drug.
“[The increase in cell numbers] was associated with an increased proliferative capacity after injury induced by scratch and with a reduction in cell death at all analyzed time points, suggesting that tadalafil promotes both cell cycle progression and cell survival,” write the researchers.
There is an interesting twist to the study results: Cells treated with tadalafil were actually less likely to mature into actual muscle fibers after a week of analysis.
The researchers interpret this as a benefit, because it means a bigger reserve of muscle stem cells are produced and ready for action. However, further studies will be needed to determine exactly how this affects muscle building (myogenesis).
“Future research should focus on in vivo models to determine if this delayed differentiation eventually leads to superior myofiber quality and to establish whether the combination of tadalafil and mechanical loading (exercise) can definitively ‘unlock’ the myogenic program for enhanced functional recovery,” write the researchers.
While there are already decades of research behind this study, there’s also still a long way to go before we know how all of this affects muscles in humans. The hope is that eventually, we may have new solutions for those with muscle-wasting diseases, or who have conditions which confine them to a bed.
The researchers say there’s also the possibility that the mechanisms triggered by tadalafil mean that it needs to be banned in sports. It’s already being used by athletes to improve blood flow and muscle function.
“Tadalafil promoted a highly proliferative state and [prevented] premature differentiation,” write the researchers. “These findings suggest its potential use as an adjuvant pharmacological therapy in the treatment of muscle-wasting disorders.”
“However, the potent improvement of muscle regenerative machinery raises critical concerns regarding its potential misuse as a performance-enhancing drug in sport, highlighting the need for evaluation by anti-doping agencies.”
The research has been published in Molecular Biology Reports.
This article was fact-checked by Fiona MacDonald and edited by Fiona MacDonald. While we pride ourselves on our process, we are only human. If you spot a mistake, please let us know.
