Mechanism of Ursolic Acid Inhibiting Myocardial Injury in Mice

2021 ◽  
Vol 11 (9) ◽  
pp. 1799-1804
Author(s):  
Hongbing Xiao ◽  
Wei Hu ◽  
Jun Gu ◽  
Dandan Li
Keyword(s):  
Ursolic Acid ◽  
Myocardial Injury ◽  
Morphological Structure ◽  
Acid Group ◽  
The Body ◽  
Myocardial Tissue ◽  
Sham Operation ◽  
Group Model ◽  
Model Group ◽  
Sham Operation Group

Ursolic acid can clear free radicals and prevent the formation of non-enzymatic glycosylation products. Our study assessed the inhibitory effect of UA on the myocardial tissue of mice. 36 healthy mice were equally and randomly divided into 3 groups by double blind method, sham operation group, model group and ursolic acid group. Myocardial injury model was established and treated with ursolic acid followed by analysis of cell morphological structure and apoptosis; levels of serum CK, AST, LDH activity and IL-6, IL-1β and TNF-α levels, as well as expression of p-AKT, AKT and PI3K in myocardial tissue. The morphological structure and apoptosis of ursolic acid group were improved compared to model group (P < 0.05). CK, AST, LDH, p-AKT and PI3K level in serum of ursolic acid group was significantly decreased (P <0.05) along with significantly downregulate IL-6, IL-1β, TNF-α (P <0.05). Ursolic acid ameliorates myocardial injury in mice possibly through inhibition of AKT/P13K signaling pathway to reduce inflammatory cascade in the body.

scholarly journals Oleanolic Acid Ameliorates Aβ25-35 Injection-induced Memory Deficit in Alzheimer’s Disease Model Rats by Maintaining Synaptic Plasticity

2018 ◽  
Vol 17 (5) ◽  
pp. 389-399 ◽  
Author(s):  
Kai Wang ◽  
Weiming Sun ◽  
Linlin Zhang ◽  
Wei Guo ◽  
Jiachun Xu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Oleanolic Acid ◽  
Memory Deficit ◽  
Sham Operation ◽  
Group Model ◽  
Model Group ◽  
Sham Operation Group ◽  
Operation Group

Background: Abnormal amyloid β (Aβ) accumulation and deposition in the hippocampus is an essential process in Alzheimer’s disease (AD). Objective: To investigate whether Oleanolic acid (OA) could improve memory deficit in AD model and its possible mechanism. Methods: Forty-five SD rats were randomly divided into sham operation group, model group, and OA group. AD models by injection of Aβ25-35 were built. Morris water maze (MWM) was applied to investigate learning and memory, transmission electron microscope (TEM) to observe the ultrastructure of synapse, western blot to the proteins, electrophysiology for long-term potentiation (LTP), and Ca2+ concentration in synapse was also measured. Results: The latency time in model group was significantly longer than that in sham operation group (P=0.0001); while it was significantly shorter in the OA group than that in model group (P=0.0001); compared with model group, the times of cross-platform in OA group significantly increased (P=0.0001). TEM results showed OA could alleviate neuron damage and synapses changes induced by Aβ25-35. The expressions of CaMKII, PKC, NMDAR2B, BDNF, TrkB, and CREB protein were significantly improved by OA (P=0.0001, 0.036, 0.041, 0.0001, 0.0001, 0.026, respectively) compared with that in model group; the concentration of Ca2+ was significantly lower in OA group (1.11±0.42) than that in model group (1.68±0.18); and the slope rate (P=0.0001) and amplitude (P=0.0001) of f- EPSP significantly increased in OA group. Conclusion: The present results support that OA could ameliorate Aβ-induced memory loss of AD rats by maintaining synaptic plasticity of the hippocampus.

scholarly journals Effects of Huoxue Xiaoyi Decoction on Apoptosis of Granulosa Cells in Endometriosis Rats

2020 ◽  
Author(s):  
Guang Shi ◽  
Yong Liu ◽  
Ruihua Zhao ◽  
Weiwei Sun ◽  
Qian Han ◽  
...  
Keyword(s):  
Granulosa Cells ◽  
Caspase 3 ◽  
Follicular Development ◽  
Sham Operation ◽  
Group Model ◽  
Model Group ◽  
Blank Group ◽  
Sham Operation Group ◽  
Ovarian Granulosa Cells ◽  
Operation Group

Abstract Background: Endometriosis(EM) is a common disease that occurs in reproductive age. 50% endometriosis patients is suffering from infertility. Follicular development is the main cause of endometriosis-associated infertility. Here the study based on apoptosis of granulosa cells during follicular development will explore the effect and the possible mechanism of Huoxue Xiaoyi Decoction (HXXYD) on apoptosis of ovarian granulosa cells in endometriosis model rats. Methods: Thirty 8-week-old female SD rats were divided into four groups: blank group, sham-operation group, model group and HXXYD group. Blank group, sham-operation group and model group were given double-distilled water, while HXXYD group were given HXXYD for 15 days. After intragastric administration, blood samples from abdominal aorta of rats were collected to detect oxidative and antioxidative indexes including ROS, T-SOD, CAT. The morphology of follicles were observed by H&E staining and every stage of follicles were calculated. The location of granulosa cells and apoptosis related factors including Bax, Bcl-2, caspase-3 were stained by immunohistochemistry staining. The apoptosis of granulosa cells were stained by TUNEL staining and the rate of apoptosis were calculated. Apoptosis related proteins including p-JNK, Bax, Bcl-2, caspase-3 were detected by Western blot. Results: The level of serum ROS decreased, and the levels of serum T-SOD and CAT increased in the HXXYD group. The number of secondary follicles increased in HXXYD group. The expression of Bax, caspase-3 in ovarian granulosa cells decreased and the expression of Bcl-2 increased in the HXXYD group with immunochemical staining. The apoptosis rate of ovarian granulosa cells in the HXXYD group decreased. The expression of p-JNK, Bax and caspase-3 protein decreased, the expression of Bcl-2 increased in the HXXYD group.Conclusions: These results indicate that HXXYD may improve the oxidative stress state, decrease the apoptosis of ovarian granulosa cells, and improve the development of follicles in endometriosis model rats through ROS-JNK signaling pathway.

scholarly journals The effect of lithium chloride on the motor function of spinal cord injury–controlled rat and the relevant mechanism

2019 ◽  
Vol 17 ◽  
pp. 205873921985285
Author(s):  
Gang Chen ◽  
Yimin Liang ◽  
Fanghu Chen ◽  
Haifeng Wang ◽  
Guoming Zhu
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Lithium Chloride ◽  
Sham Operation ◽  
Model Group ◽  
Nissl Staining ◽  
Sham Operation Group ◽  
Significant Difference ◽  
Cord Injury ◽  
Operation Group

The objective of this study is to discuss the effect and mechanism of lithium chloride on the rehabilitation of locomotion post spinal cord injury (SCI) by observing the effect of lithium chloride on the expression of the brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB) pathway. In total, 36 Sprague-Dawley (SD) rats were randomly divided into the sham operation group (n = 12), model group (n = 12), and lithium chloride group (n = 12). The sham operation group underwent laminectomy, while for the model group and the lithium chloride group with the NYU spinal cord impactor the SCI model was established. Basso, Beattie, and Bresnahan (BBB) score was used to evaluate locomotion after administration for 1, 3, 5, and 7 days, and the tissues were gathered for Nissl staining, transmission electron microscopy, immunofluorescence, and Western blot. With a statistical difference ( P < 0.05) on the 3rd day and significant difference ( P < 0.01) on the 5th day post administration, a higher BBB score was observed in the lithium chloride group indicating that lithium chloride improved the locomotion function after SCI. A better structure and morphology of neuron were observed by Nissl staining in the lithium chloride group. Lithium chloride promoted BDNF secretion from neurons in the spinal cord anterior horn with a significant difference compared to the model group ( P < 0.01). Compared with the model group, lithium chloride significantly promoted the expression of BDNF protein and phosphorylated TrkB protein ( P < 0.05), but no difference in the expression of TrkB was detected. Lithium chloride can alleviate the locomotion function after SCI with a mechanism that it can promote BDNF secretion from neurons in the spinal cord anterior horn and phosphorylation of TrkB to upregulate the BDNF/TrkB pathway supporting survival of neurons and regeneration and remyelination of axons.

scholarly journals Luhong Formula Has a Cardioprotective Effect on Left Ventricular Remodeling in Pressure-Overloaded Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Qian Liu ◽  
Hui-Yan Qu ◽  
Hua Zhou ◽  
Jing-Feng Rong ◽  
Tian-Shu Yang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Caspase 3 ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Sham Operation ◽  
Model Group ◽  
Enos Expression ◽  
Sham Operation Group ◽  
Operation Group

Background. Luhong formula (LHF)—a traditional Chinese medicine containing Cervus nippon Temminck, Carthamus tinctorius L., Astragalus membranaceus (Fisch.) Bge. var. mongholicus (Bge.) Hsiao, Codonopsis pilosula (Franch.) Nannf., Cinnamomum cassia Presl, and Lepidium apetalum Willd—is used in the treatment of heart failure, but little is known about its mechanism of action. We have investigated the effects of LHF on antifibrosis. Methods. Forty-eight SD male rats were randomly assigned into six groups (n = 8), model group, sham-operation group, perindopril group (0.036 mg/ml), LHF high doses (LHF-H, 1.44 g/mL), LHF middle doses (LHF-M, 0.72 g/mL), and LHF low doses (LHF-L, 0.36 g/mL). Except the sham-operation group, the other groups were received an abdominal aorta constriction to establish a model of myocardial hypertrophy. The HW and LVW were measured to calculate the LVW/BW and HW/BW. ELISA was used to detect the serum concentration of BNP. The expressions of eNOS, TGF-β1, caspase-3, VEGF, and VEGFR2 in heart tissues were assessed by western blot analysis. mRNA expressions of eNOS, Col1a1, Col3a1, TGF-β1, VEGF, and VEGFR2 in heart tissues were measured by RT-PCR. The specimens were stained with hematoxylin-eosin (HE) and picrosirius red staining for observing the morphological characteristics and collagen fibers I and III of the myocardium under a light microscope. Results. LHF significantly lowered the rat’s HW/BW and LVM/BW, and the level of BNP in the LHF-treated group compared with the model group. Histopathological and pathomorphological changes of collagen fibers I and III showed that LHF inhibited myocardial fibrosis in heart failure rats. Treatment with LHF upregulated eNOS expression in heart tissue and downregulated Col1a1, Col3a1, TGF-β1, caspase-3, VEGF, and VEGFR2 expression. Conclusion. LHF can improve left ventricular remodeling in a pressure-overloaded heart failure rat model; this cardiac protective ability may be due to cardiac fibrosis and attenuated apoptosis. Upregulated eNOS expression and downregulated Col1a1, Col3a1, TGF-β1, caspase-3, VEGF, and VEGFR2 expression may play a role in the observed LHF cardioprotective effect.

Research on Action of Bone Marrow Stromal Cells (BMSC) Modified by Toll-Like Receptor for Myocardial Function of Rats with Myocardial Infarction (MI)

2021 ◽  
Vol 11 (9) ◽  
pp. 1832-1837
Author(s):  
Zhongkui Li ◽  
Wenbo Liu ◽  
Lufang Gao ◽  
Daokang Xiang
Keyword(s):  
Myocardial Function ◽  
Regulatory Action ◽  
Sham Operation ◽  
Toll Like Receptor ◽  
Model Group ◽  
Degree Of Deformation ◽  
Sham Operation Group ◽  
Sd Rats ◽  
Tlr4 Agonist ◽  
Operation Group

MI could affect myocardial function seriously. The action and mechanism of BSMC modified by the transplantation of Toll-like receptor on myocardial function of rats with MI was studied. The sixty SD rats were divided into sham-operation group and model group randomly. The isolated and cultivated BMSC was divided into three groups such as group with added by TLR4 agonist, group with added by TLR-4 antagonist as TAK-242, group with only BMSC. The model of rats with MT was established in model group. BMSC in different group was transplanted into rats respectively. The cardiac function of rats in sham-operation group and model group was observed. The distribution condition of surface molecule in BMSC was detected by FCM. There was expression CD44 (+), CD54 (+), CD90 (+), no expression CD34 (−) from results. It could indicated that BMSCs with high purity was cultivated successfully. The high MT expression was affected by TLR-4 generally which could also illustrate the degree of deformation and necrosis of cardiac muscle cell, could be enhanced in established rat model because of negative regulatory action. The zone of MI in rats could be amplified by TLR-4. The cytobiological function of BMSC could be adjusted by TLR-4 through the transplantation of TLR-4 after there was MI in rats. The cytobiological function of BMSC could be adjusted by TLR-4 through modification of the transplantation of TLT-4 in rats after there was MI in rats. The BMSCs modified by high TLR-4 expression had negative regulatory action on the treatment on MI.

Effect of Propylene Glycol Alginate Sodium Sulfate Nanoparticles on Myocardial Injury in Diabetic Rats via Silent Information Regulator 1/Hypoxia-Inducible Factor-1 Alpha Pathway

2021 ◽  
Vol 21 (2) ◽  
pp. 1351-1356
Author(s):  
Sheng Qiu ◽  
Lei Cai ◽  
Wenjing Zhao ◽  
Xiaohong Pang
Keyword(s):  
Treatment Group ◽  
Propylene Glycol ◽  
Myocardial Injury ◽  
Sodium Sulfite ◽  
Diabetic Rats ◽  
Signal Pathway ◽  
Myocardial Tissue ◽  
Model Group ◽  
Diabetic Model ◽  
Propylene Glycol Alginate

The main purpose of this paper is to study the effect of propylene glycol alginate sodium sulfite nanoparticles on myocardial injury in diabetic rats through Sirt1/HIF-1 α signal pathway. The effects of different doses of propylene glycol alginate sodium sulfite nanoparticles on the content of malondialdehyde, creatine kinase, nitric oxide, the activity of superoxide dismutase, lactate dehydrogenase and nitric oxide synthetase in the myocardial tissue of diabetic rats observed. The function indexes of HIF-1 α mitochondria and measured the expression of Sirt1/HIF-1 α pathway. The results show that compare with the diabetic model group, the blood glucose level of the rats in the propylene glycol alginate sodium sulfite nanoparticles treatment group was slightly low. The serum LDH, CK and MDA contents were significantly low, and the activity of SOD in the myocardium in the propylene glycol alginate sodium sulfite nanoparticles treatment group was significantly higher than that in the diabetic model group in the treatment group. The activity of NOS and the content of MDA and no were lower than that in the diabetic rats, the expression of Sirt1 and HIF-1α in myocardial tissue was increased. It suggested that propylene glycol alginate sodium sulfite nanoparticles alleviate myocardial damage in diabetic rats by regulating Sirt1/HIF-1α signal pathway, improving mitochondrial function and inhibiting oxidative stress.

scholarly journals The Protecting Effects and Mechanisms of Baicalin and Octreotide on Heart Injury in Rats with SAP

2007 ◽  
Vol 2007 ◽  
pp. 1-11 ◽  
Author(s):  
Zhang Xiping ◽  
Tian Hua ◽  
Chen Hanqing ◽  
Chen Li ◽  
Wang Zhiwei ◽  
...  
Keyword(s):  
Protein Expression ◽  
Caspase 3 ◽  
Treated Group ◽  
Myocardial Cell ◽  
Sham Operation ◽  
Model Group ◽  
Expression Levels ◽  
Sham Operation Group ◽  
Heart Injury ◽  
Operation Group

Purpose.To observe the protecting effects and mechanisms of Baicalin and Octreotide on heart injury in rats with severe acute pancreatitis (SAP).Methods.The SAP rat models were randomly divided into the model group, Baicalin-treated group, Octreotide treated group, and sham operation group. The contents of some inflammatory indexes in blood were determined. The rat mortality, pathological changes of heart, the changes ofNF-κB, P-Selectin, Bax, Bcl-2, and Caspase-3 protein expression levels as well as apoptotic index were observed in all groups, respectively, at 3 hours, 6 hours, and 12 hours after operation.Results.The survival rate of model group was less than treated groups at 12 hours, difference was significant. The contents of some inflammatory indexes of the treated groups were lower than those of the model group to various degrees at different time points. The pathological myocardial changes under light microscope were milder in treated groups than in model group. The changes ofNF-κB, P-Selectin, Bax, Bcl-2, and Caspase-3 protein expression levels in all groups were different. There was only a case of myocardial cell apoptosis in an Octreotide-treated group at 6 hours.Conclusion.Baicalin and Octreotide have protecting effects on heart injury of rats with SAP.

Eldecalcitol Plays a Role in Postmenopausal Osteoporosis through Mir-151a-3p/Socs5 Pathway

2021 ◽  
Vol 7 (5) ◽  
pp. 3934-3941
Author(s):  
Hongqing Zhang ◽  
Li Jia ◽  
Danzhi Li
Keyword(s):  
Postmenopausal Osteoporosis ◽  
Cell Activity ◽  
Control Group ◽  
Sham Operation ◽  
Model Group ◽  
Mineral Density ◽  
Specific Mechanism ◽  
Sham Operation Group ◽  
Model Control ◽  
Model Control Group

Objective: This study set out to explore the specific mechanism of Eldecalcitol in postmenopausal osteoporosis (PMOP) and its relationship with miR-151a-3p/SOCS5 pathway. Methods: Forty-five rats were randomly and equally divided into sham operation group (SOG), model control group (MCG) and Eldecalcitol group (EG). miR-151a-3p, SOCS5 and bone mineral density (BMD) levels in each group were detected. MC3T3-E1 cells were modeled and divided into control group (CG), model group (MG) and EG. miR-151a-3p-inhibitor and pcDNA3.1-SOCS were transfected into model cells. miR-151 A-3P, SOCS5, RANKL and OPG levels as well as cell activity of cells in each group were observed. Results: Eldecalcitol intervention in rats can reduce BMD reduction caused by PMOP, reduce the miR-151a-3p level and increase the SOCS5 level. Cell experiments found that Eldecalcitol intervention can improve cell activity, inhibit the miR-151a-3p level and promote the SOCS5 expression, all of which can improve bone resorption of model cells, increase cell activity, inhibit the RANKL level and promote the OPG level. Conclusion: Eldecalcitol plays a role in PMOP by inhibiting miR-151a-3p and promoting the SOCS5 level.

Yiqi Dingxuan Yin improves cerebral ischaemic injury in rats by inhibiting apoptosis and promoting angiogenesis

2021 ◽  
Author(s):  
Fei Liu ◽  
Liuyang Xie ◽  
Chunhua Liu ◽  
Guilian He ◽  
Chunyun Yuan ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cerebral Ischaemia ◽  
Neurological Function ◽  
Neural Function ◽  
Sham Operation ◽  
Nerve Function ◽  
Model Group ◽  
Expression Levels ◽  
Sham Operation Group ◽  
Operation Group

Abstract Background Clinically, Yiqi Dingxuan Yin promotes nerve function recovery and improves nerve function defect symptoms; however, the underlying molecular pathways remain unknown. In this study, we established a rat model of cerebral ischaemia induced by middle cerebral artery occlusion (MCAO). The effects of Yiqi Dingxuan Yin on the neurological function and local neuron morphology were compared with those of butylphthalide, which is used to treat ischemic stroke, and the possible mechanisms of action were explored. Methods Of 97 healthy adult male Sprague‒Dawley rats, 20 were randomly assigned to the sham operation group. The remaining rats underwent MCAO. Model generation was successful in 60 rats, which were randomly divided into a model group, butylphthalide group, and Yiqi Dingxuan Yin group (n = 20/group) administered distilled water, butylphthalide capsule, and Yiqi Dingxuan Yin, respectively. Zea-Longa scores were used to assess the neurological function of the rats at 1, 3, 7, and 14 days. Haematoxylin and eosin staining of brain sections was used to observe morphological changes in the rat hippocampus. Apoptosis of nerve cells was detected using TUNEL staining. The expression levels of erythropoietin/erythropoietin receptor (EPO/EPOR), vascular endothelial growth factor (VEGF), and brain-derived neurotrophic factor/tyrosine receptor kinase B (BDNF/TrkB) protein in the ischaemic brain tissue were detected using immunohistochemistry. Results The apoptosis rate, and EPO/EPOR, VEGF, and BDNF/TrkB expression levels were higher in the model group than in the sham operation group (P < 0.05). Among MCAO groups, the nerve function deficit score and cell apoptosis rate were lower (P < 0.05), whereas the EPO/EPOR, VEGF, and BDNF/TrkB protein expression levels were higher (P < 0.05) in both the butylphthalide and Yiqi Dingxuan Yin groups than in the model group. Conclusions Yiqi Dingxuan Yin can improve the neural function and morphology of neurons after cerebral ischaemia injury in rats, with a more significant effect at 14 days. This may be related to the upregulation of EPO/EPOR, VEGF, and BDNF/TrkB protein expression, which may promote angiogenesis to improve cerebral blood flow and oxygen supply, thereby protecting the form and function of neurons and promoting the restoration of impaired neural function.

scholarly journals Exploring the Mechanism of Berberine Intervention in Ulcerative Colitis from the Perspective of Inflammation and Immunity Based on Systemic Pharmacology

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Yan Jiang ◽  
Li Zhao ◽  
Qing Chen ◽  
Lihong Zhou
Keyword(s):  
Ulcerative Colitis ◽  
Protein Expression ◽  
Enrichment Analysis ◽  
The Body ◽  
Signal Pathways ◽  
Group Model ◽  
Pathological Changes ◽  
Model Group ◽  
Colon Tissue ◽  
Tnf Α

Background. Ulcerative colitis (UC) is a chronic nonspecific inflammatory disease of the colon and rectum. Recent studies found that berberine had effects on inflammatory diseases and immune diseases. Methods. The PharmMapper database was used to predict the berberine potential target and GeneCards database and OMIM database were utilized to collect UC genes. The Cytoscape software was used to construct and analyze the networks and DAVID was utilized to perform enrichment analysis. Then, animal experiments were performed to validate the prediction results. The experimental rats were randomly divided into normal group (control group), model group, and berberine group. The general condition, body weight, gross morphology of colon tissue, and colonic mucosal damage index (CMDI) score were observed. The pathological changes of colon tissue were observed by H&E staining. The levels of serum interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and IL-4 were detected by ELISA. The expressions of IL-1β, TNF-α, and IL-4 protein in colon tissue were detected by immunohistochemistry. Results. A total of 211 Berberine’s potential targets and 210 UC genes were obtained. The enrichment analysis showed that berberine may regulate inflammation, inflammatory cytokines, and their mediated inflammation signal pathways such as inflammatory bowel disease (IBD), rheumatoid arthritis, cytokine-cytokine receptor interaction, TNF, T cell receptor, Toll-like receptor, and JAK/STAT signaling pathway. Compared with the model group, the body mass of rats in the berberine group was significantly increased ( P  < 0.05); the general morphology and pathological changes of colon tissue were significantly improved; CMDI score, serum and colon tissue IL-1β, TNF-α content, and protein expression were decreased significantly ( P  < 0.05); and IL-4 content and protein expression increased significantly ( P  < 0.05). Conclusion. Berberine can interfere with UC through related biological processes and signal pathways related to inflammation and immunity. In-depth exploration of the mechanism of berberine in the treatment of UC will provide a basis for clinical application.

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