scholarly journals Pachymic acid inhibits inflammation and cell apoptosis in lipopolysaccharide (LPS)-induced rat model with pneumonia by regulating NF-κB and MAPK pathways

2021 ◽  
Vol 49 (5) ◽  
pp. 876-93
Author(s):  
Yanjun Gui ◽  
Lijuan Sun ◽  
Rui Liu ◽  
Jinzhu Luo
Keyword(s):  
Cell Apoptosis ◽  
Lung Parenchyma ◽  
High Morbidity ◽  
Rat Lung ◽  
Histopathological Changes ◽  
Anticancer Properties ◽  
Mapk Pathways ◽  
Common Infectious Disease ◽  
Pachymic Acid ◽  
Triterpene Compound

Pneumonia is a common infectious disease with high morbidity and mortality. It is caused by a variety of pathogenic microorganisms that infect the lung parenchyma. Anti-infective drugs are one of the preferred choices for the treatment of pneumonia. Pachymic acid (PA) is a lanolin triterpene compound from Poria cocos, which has antiemetic, anti-inflammatory, and anticancer properties. Although PA inhibits inflammatory response in a variety of diseases, its role in pneumonia is not clear. In this study, we established that PA improved histopathological changes in the lungs of rats with pneumonia. PA inhibited the expression of inflammatory cytokines in the serum of rats having pneumonia. In addition, PA inhibited the apoptosis of cells from rat lung tissues. Mechanically, PA inhibited inflammation and cell apoptosis via NF-κB and MAPK pathways. Therefore, PA could serve as a promising drug for treating pneumonia.

scholarly journals Fibroblast Growth Factor-2 and Receptor-1α(IIIc) Regulate Postnatal Rat Lung Cell Apoptosis

2006 ◽  
Vol 174 (5) ◽  
pp. 581-589 ◽  
Author(s):  
Man Yi ◽  
Rosetta Belcastro ◽  
Samuel Shek ◽  
Daochun Luo ◽  
Martin Post ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Cell Apoptosis ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Rat Lung

Silymarin augments human cervical cancer HeLa cell apoptosis via P38/JNK MAPK pathways in serum-free medium

2005 ◽  
Vol 7 (5) ◽  
pp. 701-709 ◽  
Author(s):  
Qing Huang ◽  
Li-Jun Wu ◽  
Shin-Ichi Tashiro ◽  
Satoshi Onodera ◽  
Lin-Hao Li ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Hela Cell ◽  
Cell Apoptosis ◽  
Serum Free Medium ◽  
Free Medium ◽  
Serum Free ◽  
Mapk Pathways ◽  
Human Cervical Cancer

scholarly journals Probabilistic predictive mathematical model of chronic respiratory conditions to reduce the risk of disability in case of poisoning with substances with a pulmonotoxic effect.

2019 ◽  
Vol 21 (3) ◽  
pp. 23-29
Author(s):  
N G Vengerovich ◽  
M A Yudin ◽  
Yu O Konshakov ◽  
S V Chepur ◽  
I M Ivanov
Keyword(s):  
Mathematical Model ◽  
Pulmonary Toxicity ◽  
Structural Changes ◽  
Lung Parenchyma ◽  
Histopathological Changes ◽  
Acute Period ◽  
Icd 10 ◽  
Respiratory State ◽  
Severe Degree ◽  
Respiratory Conditions

In the experimental model of poisoning of rats with phosgene of severe degree (single administration in Tox dose 1 of Lt50 - 3.92 mgґmin/l), the parameters of the respiratory system and histopathological changes of the lung parenchyma were investigated. It was established that 45 days after exposure to phosgene, half of the surviving animals formed a complex of persistent physiological, functional, and structural changes in the syndrome of the syndrome and the chronic respiratory state (J68.4 ICD-10). The main independent predictors from the number of laboratory and functional parameters in the acute period of pulmonary toxicant poisoning (6 hours) were established by the method of mathematical analysis, on the basis of which a model was developed to predict the likelihood of chronic respiratory states in poisoned animals as consequences of severe phosgene poisoning. It is shown that an increase in the concentration of lipid peroxidation products in the blood plasma by 25% determines the likelihood of late effects of more than 0.95. The obtained mathematical model will allow predicting the characteristics of the flow of affected, in need of emergency medical prevention of chronic respiratory conditions in the provision of medical care in the acute period of pulmonary toxicity poisoning.

scholarly journals Inhibition of vitamin D analog eldecalcitol on hepatoma in vitro and in vivo

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 663-671
Author(s):  
Limin Ye ◽  
Liyi Zhu ◽  
Jinglin Wang ◽  
Fei Li
Keyword(s):  
Cell Cycle ◽  
Vitamin D ◽  
Cell Apoptosis ◽  
Control Group ◽  
High Morbidity ◽  
Rt Pcr ◽  
Vitamin D Analog ◽  
E Cadherin ◽  
Cycle Detection

AbstractHepatoma is a serious liver cancer with high morbidity and mortality. Eldecalcitol (ED-71), a vitamin D analog, is extensively used as anti-cancer agent in vitro. Hepatocellular carcinoma cell, SMMC-7721 cell lines were used in this study. Transwell assay, cell apoptosis and cell cycle detection assays were investigated after treatment with ED-71 and phosphate buffered saline (PBS) as control. Sizes of tumors were measured after ED-71 treatment in a mouse model. E-cadherin and Akt gene expressions were detected by real-time PCR (RT-PCR). The results showed that cell invasion and migration were decreased markedly after ED-71 treatment compared to control group. Cell cycle detection showed that the G2 stage was 13.18% and total S-stage was 41.16% in the ED-71 group and G2 stage: 22.88%, total S-stage: 27.34% in the control group. Cell apoptosis rate was promoted in the ED-71 group. Size of the tumors reduced more after the ED-71 treatment than the PBS treatment in mice. ED-71 markedly inhibited the expression of Akt and E-cadherin, either detected by immunohistochemistry or RT-PCR. ED-71 treatment can inhibit the hepatoma agent proliferation by increasing the E-cadherin expression and decreasing Akt expression. Therefore, these findings provide novel evidence that ED-71 can be used as an anti-hepatoma agent.

Ligustrazine alleviates acute pancreatitis by accelerating acinar cell apoptosis at early phase via the suppression of p38 and Erk MAPK pathways

2016 ◽  
Vol 82 ◽  
pp. 1-7 ◽  
Author(s):  
Jianli Chen ◽  
Junmao Chen ◽  
Xiaotao Wang ◽  
Changyou Wang ◽  
Wenbin Cao ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Acinar Cell ◽  
Cell Apoptosis ◽  
Early Phase ◽  
Erk Mapk ◽  
Mapk Pathways
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