Transient Analysis of the Therapeutic Effect of Turbulence Laser Medicine in the Treatment of Pathological Changes in TMJ Due to Occlusal Trauma

2021 ◽  
pp. 34-68
Author(s):  
J. Kamenoff
Keyword(s):  
Therapeutic Effect ◽  
Transient Analysis ◽  
Pathological Changes ◽  
Laser Medicine

Atractylenolide II-ameliorated hyperlipidemia in mice by regulating AMPK/PPARα/SREBP-1C signaling pathway

2019 ◽  
Vol 9 (5) ◽  
pp. 517-523 ◽  
Author(s):  
Qi Ren ◽  
Ge Fang ◽  
Bin Wang ◽  
Xiaowen Zhou ◽  
Xiantao Li
Keyword(s):  
Body Weight ◽  
Signaling Pathway ◽  
Therapeutic Effect ◽  
Blood Lipids ◽  
Therapeutic Agents ◽  
Enzyme Linked Immunosorbent Assay ◽  
Pathological Changes ◽  
Reduced Body ◽  
Hematoxylin And Eosin ◽  
Hematoxylin And Eosin Staining

In this paper, we present our study on the effect of atractylenolide II on hyperlipidemic model mice. After 8 weeks, the blood of these mice was taken to detect four lipids. Pathological changes were detected in the aortas and livers of the mice. Expression of PPARα and SREBP-1C was detected in the liver by western blot. An enzyme-linked immunosorbent assay was used to detect the effects of atractylenolide II on blood lipids in hyperlipidemia mice. Hematoxylin and eosin staining was used to detect pathological changes in the aortas and livers of mice with hyperlipidemia after treatment with atractylenolide II. Changes in PPARα and SREBP-1C expression were found in mice with dyslipidemia. As the results shown, atractylenolide II administration reduced body weight and hyperlipidemia in hyperlipidemic model mice. In addition, atractylenolide II effectively relieved fat deposition and damage in aortic and liver tissues. Therefore, atractylenolide II had a beneficial therapeutic effect in reducing hyperlipidemia in hyperlipidemic model mice, which may be related to its ability to inhibit SREBP-1C expression by activating PPARα. The molecular mechanism driving the therapeutic effect of atractylenolide II may involve upregulation of PPARα and activation of the AMPK/PPARα/SREBP-1C signaling pathway. Our research demonstrated the development of therapeutic agents that can be used to improve hyperlipidemia.

Pathological changes of frozen shoulder in rat model and the therapeutic effect of PPAR‐γ agonist

2020 ◽  
Author(s):  
Jinfu Chen ◽  
Junjun Zhu ◽  
Tianfei Zhu ◽  
Jiaming Cui ◽  
Zhenhan Deng ◽  
...  
Keyword(s):  
Therapeutic Effect ◽  
Rat Model ◽  
Frozen Shoulder ◽  
Pathological Changes ◽  
Ppar Γ

scholarly journals Therapeutic Effect of MG132 on the Aortic Oxidative Damage and Inflammatory Response in OVE26 Type 1 Diabetic Mice

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Xiao Miao ◽  
Wenpeng Cui ◽  
Weixia Sun ◽  
Ying Xin ◽  
Bo Wang ◽  
...  
Keyword(s):  
Therapeutic Effect ◽  
Chronic Treatment ◽  
Low Dose ◽  
Matched Control ◽  
Related Factor ◽  
Nuclear Factor ◽  
Diabetic Mice ◽  
Pathological Changes ◽  
Nrf2 Expression

The present study tested whether MG132 increases vascular nuclear factor E2-related factor-2 (Nrf2) expression and transcription to provide a therapeutic effect on diabetes-induced pathogenic changes in the aorta. To this end, three-month-old OVE26 diabetic and age-matched control mice were intraperitoneally injected with MG-132, 10 μg/kg daily for 3 months. OVE26 transgenic type 1 diabetic mice develop hyperglycemia at 2-3 weeks of age and exhibit albuminuria at 3 months of age with mild increases in TNF-αexpression and 3-NT accumulation in the aorta. Diabetes-induced significant increases in the wall thickness and structural derangement of aorta were found in OVE26 mice with significant increases in aortic oxidative and nitrosative damage, inflammation, and remodeling at 6 months of diabetes, but not at 3 months of diabetes. However, these pathological changes seen at the 6 months of diabetes were abolished in OVE26 mice treated with MG-132 for 3 months that were also associated with a significant increase in Nrf2 expression in the aorta as well as transcription of downstream genes. These results suggest that chronic treatment with low-dose MG132 can afford an effective therapy for diabetes-induced pathogenic changes in the aorta, which is associated with the increased Nrf2 expression and transcription.

scholarly journals Therapeutic effect of concentrated growth factor preparation on skin photoaging in a mouse model

2020 ◽  
Vol 48 (10) ◽  
pp. 030006052096294
Author(s):  
Rongrong Zhou ◽  
Miao Wang ◽  
Xudong Zhang ◽  
Aifen Chen ◽  
Yanghonghong Fei ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mouse Model ◽  
Therapeutic Effect ◽  
Nude Mouse ◽  
Pathological Changes ◽  
Regeneration System ◽  
Nude Mouse Model ◽  
Expression Levels ◽  
Skin Photoaging ◽  
Positive Controls

Objective To establish a nude mouse model of photoaging and study the therapeutic effect of a concentrated growth factor preparation (CGF) on skin photoaging. Methods CGF was prepared from blood from Sprague–Dawley rats. A skin photoaging nude mouse model was developed using UV irradiation combined with the photosensitizer, 8-methoxypsoralen. Mice were divided randomly into seven groups (n = 6 per group): normal control, photoaging, mock treatment, saline treatment, CGF treatment, Filoca 135HA treatment, and plasma skin regeneration system irradiation (the latter two were positive controls). Body weight and skin appearance were observed and pathological changes were determined by hematoxylin and eosin staining. Fiber elasticity was evaluated by Weigert staining. Expression levels of proliferating cell nuclear antigen (PCNA) and matrix metalloproteinase 1 (MMP1) were determined by immunohistochemistry. Results A mouse model with typical features of photoaging skin was successfully developed. CGF significantly improved the skin appearance, wrinkle scores, pathological changes, and fiber elasticity, and increased PCNA and decreased MMP1 expression levels in photoaging mice, comparable to the two positive controls. Conclusion CGF can improve the symptoms of skin photoaging in mice, suggesting that it may have applications in the treatment of skin aging in humans.

Preparation and Treatment for Oral Ulcer of Quercetin and the Drug-Loaded Chitosan Composite Material

2012 ◽  
Vol 583 ◽  
pp. 44-48
Author(s):  
Lan Guo ◽  
Zhi Yu Zhao ◽  
Jing Bai ◽  
Shu Ying Han
Keyword(s):  
Composite Material ◽  
Composite Film ◽  
Therapeutic Effect ◽  
Rat Model ◽  
Oral Ulcer ◽  
Pathological Changes ◽  
Film Forming ◽  
Chitosan Composite

With the drug-loaded chitosan as film forming materials, use salivation method to prepare Quercetin-chitosan composite film of oral ulcer and use this film to the treatment for the rat model of oral ulcer. To study the therapeutic effect for oral ulcer of the Quercetin-Chitosan composite film by measuring the area, the volume and the healing speed of the ulcer, observing edema and congestion degree of ulcer surface, and detecting the pathological changes of ulcer tissue by HE staining.

Reversal of cardiomyopathy resulting from prenatal exposure to ethanol

1984 ◽  
Vol 42 ◽  
pp. 716-717
Author(s):  
C. Uphoff ◽  
C. Nyquist-Battie
Keyword(s):  
Prenatal Exposure ◽  
Heart Development ◽  
Membrane Integrity ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Pathological Changes ◽  
Prenatally Exposed ◽  
Inner Mitochondrial Membrane ◽  
Fetal Alcohol ◽  
Newborn Mice

Fetal Alcohol Syndrone (FAS) is a syndrome with characteristic abnormalities resulting from prenatal exposure to ethanol. In many children with FAS syndrome gross pathological changes in the heart are seen with septal defects the most prevalent abnormality recorded. Few studies in animal models have been performed on the effects of ethanol on heart development. In our laboratory, it has been observed that prenatal ethanol exposure of Swiss albino mice results in abnormal cardiac muscle ultrastructure when mice were examined at birth and compared to pairfed and normal controls. Fig. 1 is an example of the changes that are seen in the ethanol-exposed animals. These changes include enlarged mitochondria with loss of inner mitochondrial membrane integrity and loss of myofibrils. Morphometric analysis substantiated the presence of these alterations from normal cardiac ultrastructure. The present work was undertaken to determine if the pathological changes seen in the newborn mice prenatally exposed to ethanol could be reversed with age and abstinence.

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