子宫内膜纤维化是各种原因所致子宫内膜损伤的共同病理特征，也是引发宫腔粘连（IUA）导致继发性不孕的主要原因。因此，如何延缓、抑制或逆转子宫内膜纤维化，是目前研究的焦点与难点。研究表明，NLRP3在子宫内膜炎症反应中起关键作用，并能调控MMPs/TIMPs，诱导细胞外基质（ECM）沉积，但具体机制不明。前期研究发现：慢性子宫内膜炎模型大鼠子宫有大量胶原增生，MMP-9表达降低，IL-1β及TIMP-1表达升高，并伴随TGF-β/smad通路的激活，而菝葜能抑制这一过程。进一步实验发现：其主要活性成分—落新妇苷能显著抑制大鼠子宫内膜炎症，并能抑制人子宫内膜间质细胞焦亡引起的IL-1β及ECM主要成分-CollagenI的表达升高。基于此，本研究拟探讨细胞焦亡能否激活TGF-β1/Smad通路进而调控MMPs/TIMPs诱导ECM沉积，并通过落新妇苷的干预寻求其作用靶点，为IUA的防治提供新思路

Endometrial fibrosis is a common pathological feature of endometrial damage caused by various causes, which is also the main cause of secondary infertility caused by intrauterine adhesions (IUA).Therefore, how to delay, inhibit or reverse endometrial fibrosis is the focus and difficulty of current research. Studies have shown that NLRP3 plays a key role in regulating the early inflammatory response of endometrial injury and can regulate the balance of MMPs/TIMPs. and can regulate MMPs / TIMPs and induce extracellular matrix (ECM) deposition, but the mechanism is unknown. Our previous studies showed that there were large amount of collagens in endometrium of Endometritis model rats, with the decreased MMP-9 expression and increased IL-1β and TIMP-1 expression. Smilax china L. could inhibit this process, but the specific mechanism was unknown.Further studies revealed that astilin, which is the main active ingredient in Smilax china L. can significantly inhibit endometrial inflammation in rats and expression of IL-1β and Collagen I caused by pyroptosis of human endometrial stromal cells. Based on this, we adopt to investigate whether pyroptosis can activate the TGF-β1/Smad pathway regulating MMPs/TIMPs-induced ECM deposition, and revealing the molecular mechanism of astilbin on the above process, providing new strategies and ideas for the prevention and treatment of IUA.