Objective To observe the pathological changes of major organs in rats with acute Dysosma versipellis poisoning and investigate the toxic mechanismand the injuries of target tissues and organs. Methods Forty Sprague-Daw ley (SD) rats were random ly divided into three experimental groups, which were given the gavage with 0.5, 1.0 and 2.0LD50 doses of Dysosma versipellis decoction, and one con-trol group, which was given the gavage with 1.0LD50 dose of normal saline. The rats were sacrificed 14 days after Dysosma versipellis poisoning and sam ples including brain, heart, liver, lung, and kidney were taken. After pathological process, the pathological changes of the major organs and tissues were observed by light microscope and electron microscope. The experimental data were statistical analyzed by x2 test. Results The observations of light microscopy: loose cytoplasmof neurons with loss of most Nissl bodies;swelling of m yocardial cells with disappearance of intercalated disk and striations;hepato-cellular edema with ballooning degeneration; and swelling epithelial cells of renal proximal convoluted tubule with red light coloring protein-like substances in the tube. The observations of electron microscopy:the structures of cell mem brane and nuclear mem brane of neurons were destroyed;cytoplasmof neurons, obvious edema;and most organelles, destroyed and disappeared. The mortalities of rats after acute poi-soning of the four groups increased with doses (P<0.05). Conclusion Acute Dysosma versipellis poisoning can cause multi-organ pathological changes. There is apositive correlation between the toxic effect and the dosage. The target tissues and organs are brain (neurons), heart, liver and kidney.

Objective:To investigate the clinical value of Rotarex ? S in debulking the femoropopliteal calcified lesion. Methods:The data of 5 patients with femoropopliteal calcified lesions treated with Rotarex ? S combined with drug balloon treatment admitted to the First Affiliated Hospital of Dalian Medical University from March 2020 to December 2021 were retrospectively analyzed. The success rate and complications of all operations were recorded. CT software was used to compare the effective lumen area of the target lesion area before and after surgery in all cases, and the ischemic grade of the affected limb before and after surgery was recorded in all patients. Results:All 5 femoropopliteal calcified lesions were successfully treated with Rotarex ? S debulking followed with drug-coated balloon angioplasty without flow-limited dissections, vascular perforation and distal embolizations, with a success rate of 100%. The effective lumen area for calcified lesions were increased 9-15.11 mm 2 (median: 13 mm 2). The Rutherford classifications were improved from R 2-4 to R 1-2. Conclusions:Femoropopliteal calcified lesion debulking with Rotarex ? S was safe and effective.

Objective : To investigate ellect of salidroside on the function and activation of rheumatoid arthritis fibroblast-like synoviocyte(HFLS-RA)by regulating the miR-20a-5p/tissue inhibitor of metalloproteinase-2(TIMP2) axis. Methods: HFlS-RA cells were used as the research object. HFlS-RA cells were separated intocontrol group, tumor necrosis factor-a (TNF-a) group, salidroside group, inhibitor NC group, miR-20a-5p inhibitor group, salidroside + mimic NC group, and salidroside + miR-20a-5p mimic group. qRT-PCR was applied to deteet the expression of miR-20a-5p in HFIS-RA cells ; enzyme-linked immunosorbent assay( ELISA) was applied todetect the levels of interleukin-18 ( lL-1β) and IL-6 in the supermatant of HFLS-RA cells: cell counting kit-8(CCK-8) method and 5-ethynyl-2 '-deoxyuridine ( EdU) staining were applied to detect HFLS-RA cell proliferation ; scratch experiment was applied to detect HilS-RA cell migration; Western blot was applied to detect the ex.pression of 'TlMP2, CyclinD1, and matrix metalloproteinase ( MMP ) -9 proteins in HFLS-RA cells; double lucifer.ase was applied to verify the relationship between miR-20a-5p and TIMP2. Results: Compared with the control group, the expression of miR-20a-5p, the levels of lL-1β and IL-6, 0Dso value, EdU positive cell rate, scratchhealing rate, and the expression of CyclinDl and MMP-9 proteins in the TNF-α group increased, the expression of TlMP2 protein decreased ( P <0. 05 ) ; compared with the TNF-α group, the expression of miR-20a-5p, the levelsof lL.-1β and IL-6, OD450 value, EdU positive cell rate, scratch healing rate, and CyclinD1 and MMP-9 proteinsexpression decreased, the expression of TlMP2 protein increased in salidroside group ( P <0. 05 ); compared withthe 'T'NF -a group and inhibitor NC group, the expression of miR-20a-5p, the levels of IL-1 β and IL.-6, OD450 val-ue, EdU positive cell rate, seratch healing rate, and the expression of CyclinDl and MMP-9 proteins in the miR.20a-5p inhibitor group decreased, the expression of TlMP2 protein increased ( P <0. 05 ); compared with the sali.droside group and the salidroside + mimic NC group, the expression of miR-20a-5p, the levels of IL-1 β and IL-6 ,OD.so value, EdU positive cell rate, scratch healing rate, and the expression of CyelinD1 and MMP-9 proteins inthe salidroside + miR-20a-5p mimic group increased, the expression of TIMP2 protein decreased ( P < 0. 05 )There was a targeted regulatory relationship between miR-20a-5p and TIMP2. Conclusion Salidroside may inhibit TNF-α-induced HFS-RA cell proliferation , migration and infammatory response by regulating miR-20a-5p/TIMP2.