Objective This study investigated the therapeutic efficacy of Rhizoma Alisma in isoproterenol(ISO)-induced myocardial fibrosis(MF) in SD rats, with a mechanistic focus on modulation of the pyroptotic pathway. Methods Rats were randomly allocated into five groups (n=8 per group): control(NC) group, MF group, Captopril(CAP) group, low-dose Rhizoma Alisma(RAL) group, and high-dose Rhizoma Alisma(RAH) group. MF was induced via ISO administration. Serum levels of CK-MB, α-HBDH, and LDH were quantified. Cardiac tissue morphology was assessed using HE and Masson staining. Western blot analysis determined the expression levels of α-SMA, NLRP3, Caspase-1, and GSDMD proteins, while laser confocal microscopy visualized Collagen I deposition in myocardial tissue. Results ISO induction triggered severe MF in rats, evidenced by histopathological collagen deposition and elevated NLRP3, Caspase-1, and GSDMD expression. Rhizoma Alisma treatment reduced serum levels of CK-MB, α-HBDH, and LDH, ameliorated tissue damage, downregulated collagen deposition, and significantly suppressed the expression of NLRP3, Caspase-1, and GSDMD. Conclusion Rhizoma Alisma demonstrates significant efficacy in attenuating ISO-induced MF, potentially through modulation of cell pyroptosis.

Objective To study the effect of lncRNA-AK093407 (AK093407 for short) on colorectal cancer HCT-15 cells and related mechanisms. Methods Lv5 lentivirus overexpressed AK093047, and transfected siRNA to silence AK093407; qRT-PCR was used to identify the expression of AK093407; MTT and plate colony formation assays were used to detect cell proliferation; flow cytometry was used to detect cell cycle and apoptosis; wound healing assay and transwell was used to detect cell invasion and migration; qRT-PCR and Western blot were used to detect the expression of EMT-related factors. Results The expression of AK093407 increased after Lv5 lentivirus infection. Overexpression of AK093407 in colorectal cancer cells increased proliferation activity, promoted cell cycle evolution, decreased apoptosis, and enhanced migration and invasion ability. The results of qRT-PCR and Western blotting showed that the transcription and translation levels of occludin and E-cadherin were decreased (P<0.05), while β-catenin, vimentin and fibronectin were increased (P<0.05). After the AK093407 gene was silenced, the above results were opposite. Conclusion AK093407 promotes colorectal cancer cell proliferation, cell cycle, invasion and migration and inhibits apoptosis via promoting EMT.