Protective effects of ligustilide, a natural product from Aaugellica sinensis (Oliv.) Diels, in a rabbit model of endotoxic shock

Rheumatoid arthritis (RA) is a systemic and chronic autoimmune inflammatory disease characterized by severe synovial hyperplasia associated with progressive cartilage degradation. Due to the severe pain and disability caused by RA, effective therapeutic strategies that could simultaneously alleviate the inflammatory response and delay the disease progression are urgently needed. As a major alternative therapy in traditional Chinese medicine, moxibustion has been demonstrated that it could reduce the chronic inflammatory responses of a series of musculoskeletal diseases; however, whether moxibustion has protective effects on RA is still unclear. To investigate the effects of moxibustion on RA, moxibustion was applied to Zusanli (ST36) and Shenshu (BL23) acupoints in a RA rabbit model. HE staining of articular cartilage showed that moxibustion alleviated the cartilage degradation and bone destruction. In addition, moxibustion decreased the osteoclast number in RA rabbits. Real-time PCR revealed that moxibustion decreased the expression of RANKL mRNA while increased the expression of OPG mRNA, indicating a restoration of the balance between osteogenesis and osteoclastogenesis. Taken together, our results indicated that moxibustion had promising antiarthritic effects and could be an useful alternative method in RA therapeutics.

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Rapid CO breath test screening of drugs for protective effects on ribavirin-induced hemolysis in a rabbit model: a pilot study

Journal of Breath Research ◽

10.1088/1752-7155/10/3/036010 ◽

2016 ◽

Vol 10 (3) ◽

pp. 036010

Author(s):

Yong-Jian Ma ◽

Hou-De Zhang ◽

Chuang-Hong Wu ◽

Guo-Liang Zhu ◽

Yong-Qiang Ji ◽

...

Keyword(s):

Pilot Study ◽

Breath Test ◽

Rabbit Model ◽

Protective Effects

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Mechanisms and Treatment of Light-Induced Retinal Degeneration-Associated Inflammation: Insights from Biochemical Profiling of the Aqueous Humor

International Journal of Molecular Sciences ◽

10.3390/ijms21030704 ◽

2020 ◽

Vol 21 (3) ◽

pp. 704 ◽

Cited By ~ 3

Author(s):

Dmitry V. Chistyakov ◽

Viktoriia E. Baksheeva ◽

Veronika V. Tiulina ◽

Sergei V. Goriainov ◽

Nadezhda V. Azbukina ◽

...

Keyword(s):

Oxidative Stress ◽

Retinal Degeneration ◽

Aqueous Humor ◽

Rabbit Model ◽

Age Related Macular Degeneration ◽

Protective Effects ◽

Cyclooxygenase Inhibitor ◽

Degenerative Diseases ◽

Age Related ◽

Retinal Degenerative Diseases

Ocular inflammation contributes to the pathogenesis of blind-causing retinal degenerative diseases, such as age-related macular degeneration (AMD) or photic maculopathy. Here, we report on inflammatory mechanisms that are associated with retinal degeneration induced by bright visible light, which were revealed while using a rabbit model. Histologically and electrophysiologically noticeable degeneration of the retina is preceded and accompanied by oxidative stress and inflammation, as evidenced by granulocyte infiltration and edema in this tissue, as well as the upregulation of total protein, pro-inflammatory cytokines, and oxidative stress markers in aqueous humor (AH). Consistently, quantitative lipidomic studies of AH elucidated increase in the concentration of arachidonic (AA) and docosahexaenoic (DHA) acids and lyso-platelet activating factor (lyso-PAF), together with pronounced oxidative and inflammatory alterations in content of lipid mediators oxylipins. These alterations include long-term elevation of prostaglandins, which are synthesized from AA via cyclooxygenase-dependent pathways, as well as a short burst of linoleic acid derivatives that can be produced by both enzymatic and non-enzymatic free radical-dependent mechanisms. The upregulation of all oxylipins is inhibited by the premedication of the eyes while using mitochondria-targeted antioxidant SkQ1, whereas the accumulation of prostaglandins and lyso-PAF can be specifically suppressed by topical treatment with cyclooxygenase inhibitor Nepafenac. Interestingly, the most prominent antioxidant and anti-inflammatory benefits and overall retinal protective effects are achieved by simultaneous administrating of both drugs indicating their synergistic action. Taken together, these findings provide a rationale for using a combination of mitochondria-targeted antioxidant and cyclooxygenase inhibitor for the treatment of inflammatory components of retinal degenerative diseases.

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Effect of l-arginine on endothelial injury and hemostasis in rabbit endotoxin shock

Journal of Applied Physiology ◽

10.1152/jappl.2000.89.5.1811 ◽

2000 ◽

Vol 89 (5) ◽

pp. 1811-1818 ◽

Cited By ~ 23

Author(s):

Eric Wiel ◽

Qian Pu ◽

Delphine Corseaux ◽

Emmanuel Robin ◽

Régis Bordet ◽

...

Keyword(s):

Endothelial Function ◽

Tissue Factor ◽

Vascular Reactivity ◽

Endotoxic Shock ◽

Rabbit Model ◽

Coagulation Factors ◽

Endotoxin Shock ◽

Endothelial Cell Surface ◽

No Formation

To investigate whether impaired endothelial function was related to alteration of nitric oxide (NO) formation during endotoxic shock, we studied the effects of supplementation of l-arginine (l-Arg),d-arginine (d-Arg), and N G-nitro-l-arginine methyl ester (l-NAME), on endothelial function and structure in a rabbit model. Endotoxic shock was induced by a single lipopolysaccharide bolus (0.5 mg/kg iv, Escherichia coli endotoxin). Coagulation factors and expression of monocyte tissue factor were determined by functional assays. Endothelium-dependent vascular relaxation was assessed by in vitro vascular reactivity. Immunohistochemical staining (CD31) was performed to assess damaged endothelial cell surface of the abdominal aorta. These parameters were studied 5 days after the onset of endotoxic shock and were compared under three conditions: in absence of treatment, with l-Arg or d-Arg supplementation, or with l-NAME. Bothl-Arg and d-Arg significantly improved endothelium-dependent relaxation and endothelial morphological injury.l-NAME did not alter endothelial histological injury induced by lipopolysaccharide. These data indicate that arginine supplementation nonspecifically prevents endothelial dysfunction and histological injury in rabbit endotoxic shock. Moreover,l-Arg has no effect on coagulation activation and expression of monocyte tissue factor induced by endotoxic shock.

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Protective effects of a natural product, curcumin, against amyloid β induced mitochondrial and synaptic toxicities in Alzheimer's disease

Journal of Investigative Medicine ◽

10.1136/jim-2016-000240 ◽

2016 ◽

Vol 64 (8) ◽

pp. 1220-1234 ◽

Cited By ~ 57

Author(s):

P Hemachandra Reddy ◽

Maria Manczak ◽

Xiangling Yin ◽

Mary Catharine Grady ◽

Andrew Mitchell ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cell Viability ◽

Natural Product ◽

Mitochondrial Biogenesis ◽

Mitochondrial Function ◽

Mitochondrial Dynamics ◽

Amyloid Β ◽

Synaptic Activity ◽

Protective Effects

The purpose of our study was to investigate the protective effects of a natural product—‘curcumin’— in Alzheimer's disease (AD)-like neurons. Although much research has been done in AD, very little has been reported on the effects of curcumin on mitochondrial biogenesis, dynamics, function and synaptic activities. Therefore, the present study investigated the protective effects against amyloid β (Aβ) induced mitochondrial and synaptic toxicities. Using human neuroblastoma (SHSY5Y) cells, curcumin and Aβ, we studied the protective effects of curcumin against Aβ. Further, we also studied preventive (curcumin+Aβ) and intervention (Aβ+curcumin) effects of curcumin against Aβ in SHSY5Y cells. Using real time RT-PCR, immunoblotting and immunofluorescence analysis, we measured mRNA and protein levels of mitochondrial dynamics, mitochondrial biogenesis and synaptic genes. We also assessed mitochondrial function by measuring hydrogen peroxide, lipid peroxidation, cytochrome oxidase activity and mitochondrial ATP. Cell viability was studied using the MTT assay. Aβ was found to impair mitochondrial dynamics, reduce mitochondrial biogenesis and decrease synaptic activity and mitochondrial function. In contrast, curcumin enhanced mitochondrial fusion activity and reduced fission machinery, and increased biogenesis and synaptic proteins. Mitochondrial function and cell viability were elevated in curcumin treated cells. Interestingly, curcumin pre- and post-treated cells incubated with Aβ showed reduced mitochondrial dysfunction, and maintained cell viability and mitochondrial dynamics, mitochondrial biogenesis and synaptic activity. Further, the protective effects of curcumin were stronger in pretreated SHSY5Y cells than in post-treated cells, indicating that curcumin works better in prevention than treatment in AD-like neurons. Our findings suggest that curcumin is a promising drug molecule to treat AD patients.

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