Diallyl Trisulfide Enhances the Survival of Multiterritory Perforator Skin Flaps

Dong, Chengji; Chen, Zhuliu; Zhu, Linxin; Bsoul, Najeeb; Wu, Hongqiang; Jiang, Jingtao; Chen, Xuankuai; Le, Yingying; Yu, Gaoxiang; Gu, Yue; Guo, Xiaoshan; Gao, Weiyang

doi:10.3389/fphar.2022.809034

Cited by 2 publications

(1 citation statement)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 31 , 39 , 41 , 42 In addition, DATS was reported to activate the PI3K/Akt signaling, which plays an important role in the process of reparative angiogenesis. 13 , 43 To our knowledge, the present study is the first to demonstrate that H 2 S activates the PI3K/Akt pathway in LECs, similar to other cell types.…”

Section: Discussionsupporting

confidence: 61%

Hydrogen Sulfide Attenuates Lymphedema Via the Induction of Lymphangiogenesis Through a PI3K/Akt‐Dependent Mechanism

Suzuki

Shimizu

Hayashi

et al. 2022

JAHA

View full text Add to dashboard Cite

Background Accumulating evidence suggests that hydrogen sulfide ( H 2 S ), an endogenously produced gaseous molecule, plays a critical role in the regulation of cardiovascular homeostasis. However, little is known about its role in lymphangiogenesis. Thus, the current study aimed to investigate the involvement of H 2 S in lymphatic vessel growth and lymphedema resolution using a murine model and assess the underlying mechanisms. Methods and Results A murine model of tail lymphedema was created both in wild‐type mice and cystathionine γ‐lyase–knockout mice, to evaluate lymphedema up to 28 days after lymphatic ablation. Cystathionine γ‐lyase–knockout mice had greater tail diameters than wild‐type mice, and this phenomenon was associated with the inhibition of reparative lymphangiogenesis at the site of lymphatic ablation. In contrast, the administration of an H 2 S donor, diallyl trisulfide, ameliorated lymphedema by inducing the formation of a considerable number of lymphatic vessels at the injured sites in the tails. In vitro experiments using human lymphatic endothelial cells revealed that diallyl trisulfide promoted their proliferation and differentiation into tube‐like structures by enhancing Akt (protein kinase B) phosphorylation in a concentration‐dependent manner. The blockade of Akt activation negated the diallyl trisulfide–induced prolymphangiogenic responses in lymphatic endothelial cells. Furthermore, the effects of diallyl trisulfide treatment on lymphangiogenesis in the tail lymphedema model were also negated by the inhibition of phosphoinositide 3'‐kinase (P13K)/Akt signaling. Conclusions H 2 S promotes reparative lymphatic vessel growth and ameliorates secondary lymphedema, at least in part, through the activation of the Akt pathway in lymphatic endothelial cells. As such, H 2 S donors could be used as therapeutics against refractory secondary lymphedema.

show abstract

Section: Discussionsupporting

confidence: 61%

Hydrogen Sulfide Attenuates Lymphedema Via the Induction of Lymphangiogenesis Through a PI3K/Akt‐Dependent Mechanism

Suzuki

Shimizu

Hayashi

et al. 2022

JAHA

View full text Add to dashboard Cite

show abstract

Diallyl trisulfide improves spinal cord ischemia–reperfusion injury damage by activating AMPK to stabilize mitochondrial function

Sun,

Xu,

Yang

et al. 2023

J Orthop Surg Res

View full text Add to dashboard Cite

Background Spinal cord ischemia–reperfusion injury (SCII) is a catastrophic event, which can cause paraplegia in severe cases. In the reperfusion stage, oxidative stress was up-regulated, which aggravated the injury and apoptosis of neurons. As the main active ingredient of garlic, diallyl trisulfide (DATS) displays strong antioxidant capacity. However, it is unknown whether DATS can protect the neurons of SCII. Materials and methods In this study, the descending aorta at the distal end of the left subclavian artery was ligated and perfused again after 14 min. Samples including blood and spinal cord (L2–L5) were taken 24 h later for morphological and biochemical examination. Results After SCII, the rats showed motor dysfunction, increase apoptosis, malondialdehyde content, mitochondrial biogenesis and dynamic balance disorder. After the application of DATS, the adenosine monophosphate activated protein kinase (AMPK) was activated, the mitochondrial damage was improved, the oxidative stress was weakened, and the neuronal damage was recovered to some extent. However, the addition of compound C significantly weakened the protective effect of DATS. Conclusion Oxidative stress caused by mitochondrial damage was one of the important mechanisms of neuronal damage in SCII. DATS could activate AMPK, stabilize mitochondrial biogenesis and dynamic balance, and reduce neuronal damage caused by oxidative stress.

show abstract

Diallyl Trisulfide Enhances the Survival of Multiterritory Perforator Skin Flaps

Cited by 2 publications

References 65 publications

Hydrogen Sulfide Attenuates Lymphedema Via the Induction of Lymphangiogenesis Through a PI3K/Akt‐Dependent Mechanism

Hydrogen Sulfide Attenuates Lymphedema Via the Induction of Lymphangiogenesis Through a PI3K/Akt‐Dependent Mechanism

Diallyl trisulfide improves spinal cord ischemia–reperfusion injury damage by activating AMPK to stabilize mitochondrial function

Contact Info

Product

Resources

About