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Chinese Traditional and Herbal Drugs ; (24): 5011-5017, 2019.
Artigo em Chinês | WPRIM | ID: wpr-850782

RESUMO

Objective: The anti-inflammatory and anti-fibrotic effects of Sanjie Zhentong Capsule (SJZT) on chronic pelvic inflammation in rats were investigated and its underlying mechanisms were explored. Methods: Ten rats regarded as normal group with sham operation were randomly selected from 60 female SD rats, and the remaining rats were injected with phenol mucilage in the left uteri to replicate chronic pelvic inflammatory disease. On day 14, after the operation, according to body weight, the 50 rats were randomly allocated to model group, dexamethasone (DEX) group, SJZT low dose group (0.192 g/kg), SJZT middle dose group (0.384 g/kg), and SJZT high dose group (0.768 g/kg). The drugs were dissolved in 0.5% CMC-Na solution and administered respectively, while 0.5% CMC-Na solution was given to the normal and model group. After all the animals were treated by oral gavage once a day for 30 d, the blood and the left uteri were collected. The uterine tissues were fixed and stained with haematoxylin-eosin (HE) and Masson’s trichrome for histopathology examination and the concentrations of TNF-α, IL-1β, PDGF, and TIMP in serum were assayed by ELISA. The protein expression levels of p-ERK1/2, p-JNK, NF-κB p65, MMP-2, and MMP-9 in the uteri were also detected by Western blotting. Results: Compared with the model group, SJZT could effectively improve the arrangement disorder of cavity wall, reduce the degeneration and necrosis of epithelial cells, the infiltration of inflammatory cells and the congestion of lamina propria, and alleviate the proliferation of collagen fibers in lamina propria. SJZT could also reduce the concentrations of TNF-α, IL-1β, PDGF, and TIMP in serum. Moreover, the protein expression of p-ERK1/2, p-JNK, and NF-κB p65 in the uteri were inhibited significantly, and at the same time the protein expression of MMP-2 and MMP-9 was increased markedly by SJZT. Conclusion: SJZT exhibits robust anti- inflammatory and anti-fibrosis effects in chronic pelvic inflammatory disease model induced by phenol mucilage. Its mechanisms may be related to regulating NF-κB and MAPK signaling pathways, inhibiting inflammation, reducing the synthesis of extracellular matrix (ECM), increasing the degradation of ECM and promoting the repair of fibrosis.

2.
China Journal of Chinese Materia Medica ; (24): 1241-1246, 2018.
Artigo em Chinês | WPRIM | ID: wpr-687306

RESUMO

To observe the protective effect of Longxue Tongluo capsule (LTC) on human umbilical vein endothelial cells (EAhy.926 cells) injury induced by oxidized low-density lipoprotein (ox-LDL, 100 mg·L⁻¹). The effect of the cell viability of LTCin alleviating OX-LDL-induced endothelial cell injury was determined by MTT and LDH assay. The effect of LTC on lactic dehydrogenase (LDH), nitric oxide (NO), super oxide dlsmutase (SOD) and malondialdehyde (MDA) levels were detected by corresponding assay kits according to manufacturer's instruction. The effect of LTC on the protein expressions of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), p65, p-p65, IKB and p-IKB were detected by Western blot. The results showed that compared with the normal control group, the activity of EAhy.926 cells was significantly decreased, LDH leakage (<0.01) increased, NO content and SOD activity significantly decreased (<0.01, <0.05), and the expressions of ICAM-1, VCAM-1, p-p65/p65 and p-IKB(<0.05)increased.This study demonstrated that LTC had no significant effect on the growth of normal cells. The treatment with LTC significantly promoted the proliferation of vascular endothelial cells damagedby ox-LDL, decreased MDA content and LDH release, andincreased the activity of SOD and NO content. Meanwhile, ox-LDL significantly increased the expressions of ICAM-1, VCAM-1, p-p65/p65, p-IKB/IKB in Eahy.926 cells; these effects were suppressed by LTC at 1, 2 mg·L⁻¹. In conclusion, LTC has a significant protective effect on human umbilical vein endothelial cells caused by ox-LDL. This study suggested that LTC has a certain therapeutic effect on AS.

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