Post-stroke treatment of storax improves long-term outcomes of stroke in rats

Min, Zhou; Li, Dongna; Li, Lin; Zhao, Ping; Yue, Shi; Xiao, Li; Du, Yiqin; Fan, Xiang; Zhang, Meng

doi:10.1016/j.jep.2021.114467

Cited by 10 publications

(7 citation statements)

References 30 publications

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“…ST has been found to ameliorate OGD/R-induced damage to brain microvascular endothelial cells, astrocytes and cortical neuronal cells, increase cell viability, decrease LDH, TNF-α and ICAM-1 release, and reduce NF-κB expression ( Zhao et al, 2016 ; Zhang M. et al, 2018 ). It was also found that ST significantly suppressed TNF-α and IL-1β expression in brain tissue and ET-1 levels in serum, reduced the number of NF-κB/p65-positive cells, and decreased the number of activated microglia/macrophages and astrocytes while reversing their morphological change 24 h after cerebral ischemia in rats ( Zhou et al, 2021 ), and also significantly reduced hemispheric edema rates, neurological function scores and brain infarct volume ratios after cerebral ischemia in rats. These results have confirmed that ST may exert neuroprotective effects by inhibiting the NF-κB signaling pathway and thus reducing the expression of related inflammatory factors.…”

Section: Pharmacological Activitiesmentioning

confidence: 89%

“…ST can increase VEGF content in serum and Na + -K + -ATPase activity in ischemic brain tissues of CI/RI rats ( Wen et al, 2017 ). Long-term neurological studies have found that ST significantly alleviates neurological impairment starting 7 days after cerebral ischemia and continuing up to 28 days, with a significant reduction in lesion volume 28 days after stroke, as well as increasing the density of CD31 and SYP around the infarcted area ( Zhou et al, 2021 ). ⑦ Regulating the production of NO …”

Section: Pharmacological Activitiesmentioning

confidence: 99%

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Storax, A Promising Botanical Medicine for Treating Cardio-Cerebrovascular Diseases: A Review

Yuan

et al. 2021

Front. Pharmacol.

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In recent years, the incidence and mortality of cardio-cerebrovascular diseases have been increasing year by year, which has become global burden and challenge. Based on the holistic thinking of “brain disease affects the heart” and “heart disease affects the brain,” as well as the characteristics of multi-target and multi-path effects of Chinese medicine, Chinese medicine is more advantageous in the treatment of cardio-cerebrovascular diseases. As a botanical medicine, storax is known for its resuscitation, filth avoidance and pain-relieving effects in the treatment of cardio-cerebrovascular diseases. By reviewing and collating the relevant domestic and international literature in the past 10 years, we have sorted out an overview of the medicinal parts, traditional uses and chemical composition of storax. For the first time, based on the idea of “cerebral and cardiac simultaneous treatment,” the pharmacological activities and mechanisms of heart and brain protection of storax for treating cardio-cerebrovascular diseases were summarized and analyzed, showing that storax has the pharmacological effects of anti-cerebral ischemia, regulation of blood-brain barrier, bidirectional regulation of the central nervous system, anti-myocardial ischemia, anti-arrhythmia, anti-thrombosis and anti-platelet aggregation. It mainly exerts its protective effects on the brain and heart through mechanisms such as inhibition of inflammatory immune factors, anti-oxidative stress, anti-apoptosis, pro-neovascularization and regulation of NO release. On the basis of the current findings and limitations, the future research strategies and perspectives of storax are proposed, with a view to providing a reference for further application and development of this medicine, as well as contributing new thoughts and visions for the clinical application of “treating brain-heart synchronously”.

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Section: Pharmacological Activitiesmentioning

confidence: 89%

Section: Pharmacological Activitiesmentioning

confidence: 99%

Storax, A Promising Botanical Medicine for Treating Cardio-Cerebrovascular Diseases: A Review

Yuan

et al. 2021

Front. Pharmacol.

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“…The expression of HABP2 was also increased in the isolated exosomes from the blood of MCAO mice (Figure D). The expression of an astrocyte activation marker GFAP and a neuron-specific marker NeuN was evaluated by IF, and the IF results exhibited that GFAP expression increased while NeuN expression decreased in MCAO mice (Figure E). Additionally, TNF-α, IL-1β, and IL-6 levels were remarkably elevated in peripheral blood from MCAO mice (Figure F).…”

Section: Resultsmentioning

confidence: 99%

HABP2 Encapsulated by Peripheral Blood-Derived Exosomes Suppresses Astrocyte Autophagy to Exacerbate Neuroinflammatory Injury in Mice with Ischemic Stroke

Luo

Huang

et al. 2023

ACS Chem. Neurosci.

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Exosomes are shown to be involved in the regulation of neuroinflammatory injury. The current study analyzed how peripheral blood-derived exosomes affected hyaluronan-binding protein 2 (HABP2) expression to regulate neuroinflammatory injury after ischemic stroke (IS). An IS animal model was stimulated by middle cerebral artery occlusion (MCAO), followed by injection of lentivirus. Peripheral blood samples were collected from MCAO mice after different treatments. The cerebral infarction volume, astrocyte activation, and neuroinflammation were observed by TTC staining, immunofluorescence, and ELISA, respectively. HABP2 was highly expressed in the brain tissues of MCAO mice. Also, an enhancement of HABP2 was noted in their peripheral blood-derived exosomes, while loss of HABP2 in peripheral blood-derived exosomes promoted the astrocyte autophagy and reduced the release of the inflammatory factors as well as the apoptosis of neuronal cells. PAR1 overexpression reversed the effect of HABP2 loss on autophagy and neuroinflammation in MCAO mice. Additionally, the agonist of the PI3K/AKT/mTOR pathway, SC79, could also reverse the effect of sh-PAR1 on neuroinflammation. Mechanistically, HABP2 enhanced PAR1 to activate the PI3K/AKT/mTOR pathway, thereby suppressing cell autophagy. Overall, HABP2 in peripheral blood-derived exosomes can activate the PAR1/PI3K/AKT/mTOR pathway to reduce autophagy and aggravate neuroinflammatory injury after IS.

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“…Except for the control group, the other groups were injected subcutaneously with ISO dissolved in saline to induce AMI, 75 mg·kg −1 ·d −1 , 24 h apart, for 2 d. The storax oil was added dropwise to the 2% Tween-80 solution, emulsified by continuous grinding and diluted with physiological saline to the desired concentrations: 0.01, 0.02, 0.04 g/mL storax. The dosages of ISO and storax were chosen based on preliminary experiments and previous literature [ 51 , 52 ].…”

Section: Methodsmentioning

confidence: 99%

Storax Attenuates Cardiac Fibrosis following Acute Myocardial Infarction in Rats via Suppression of AT1R–Ankrd1–P53 Signaling Pathway

Yuan

et al. 2022

IJMS

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Myocardial fibrosis following acute myocardial infarction (AMI) seriously affects the prognosis and survival rate of patients. This study explores the role and regulation mechanism of storax, a commonly used traditional Chinese medicine for treatment of cardiovascular diseases, on myocardial fibrosis and cardiac function. The AMI rat model was established by subcutaneous injection of Isoproterenol hydrochloride (ISO). Storax (0.1, 0.2, 0.4 g/kg) was administered by gavage once/d for 7 days. Electrocardiogram, echocardiography, hemodynamic and cardiac enzyme in AMI rats were measured. HE, Masson, immunofluorescence and TUNEL staining were used to observe the degree of pathological damage, fibrosis and cardiomyocyte apoptosis in myocardial tissue, respectively. Expression of AT1R, CARP and their downstream related apoptotic proteins were detected by WB. The results demonstrated that storax could significantly improve cardiac electrophysiology and function, decrease serum cardiac enzyme activity, reduce type I and III collagen contents to improve fibrosis and alleviate myocardial pathological damage and cardiomyocyte apoptosis. It also found that storax can significantly down-regulate expression of AT1R, Ankrd1, P53, P-p53 (ser 15), Bax and cleaved Caspase-3 and up-regulate expression of Mdm2 and Bcl-2. Taken together, these findings indicated that storax effectively protected cardiomyocytes against myocardial fibrosis and cardiac dysfunction by inhibiting the AT1R–Ankrd1–P53 signaling pathway.

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Post-stroke treatment of storax improves long-term outcomes of stroke in rats

Cited by 10 publications

References 30 publications

Storax, A Promising Botanical Medicine for Treating Cardio-Cerebrovascular Diseases: A Review

Storax, A Promising Botanical Medicine for Treating Cardio-Cerebrovascular Diseases: A Review

HABP2 Encapsulated by Peripheral Blood-Derived Exosomes Suppresses Astrocyte Autophagy to Exacerbate Neuroinflammatory Injury in Mice with Ischemic Stroke

Storax Attenuates Cardiac Fibrosis following Acute Myocardial Infarction in Rats via Suppression of AT1R–Ankrd1–P53 Signaling Pathway

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