Hydroxysafflor yellow A exerts neuroprotective effects in cerebral ischemia reperfusion-injured mice by suppressing the innate immune TLR4-inducing pathway

Lv, Yanni; Qian, Yisong; Fu, Longsheng; Chen, Xuanying; Zhong, Haili; Wei, Xiaohua

doi:10.1016/j.ejphar.2015.11.036

Cited by 53 publications

(32 citation statements)

References 42 publications

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“…Intravenous transplantation of an immortal human microglial cell line into rat brains 48 hours following MCAO resulted in the upregulation of several neurotrophic factors, including BDNF, and anti-inflammatory cytokines, which helped with the functional recovery from ischemia [93]. Hydroxysafflor yellow A (HSYA) is a natural product and the active ingredient found in the Chinese herbal medicine Flos Carthami Tinctorii, which was recently shown to exert neuroprotective effects in cerebral ischemia by enhancing BDNF expres-sion in microglia [94,95]. In another study, intranasal delivery of BDNF was shown to increase the number of activated and phagocytotic microglia, as well as the level of cytokines and transcription factors, in order to protect brain tissue from ischemic insult and reduce neuronal injury (Figure 4) [96].…”

Section: Bdnf As a Therapeutic Agent In The Treatment Of Strokementioning

confidence: 99%

Brain-Derived Neurotrophic Factor and Its Potential Therapeutic Role in Stroke Comorbidities

et al. 2020

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With the rise in the aging global population, stroke comorbidities have become a serious health threat and a tremendous economic burden on human society. Current therapeutic strategies mainly focus on protecting neurons from cytotoxic damage at the acute phase upon stroke onset, which not only is a difficult way to ameliorate stroke symptoms but also presents a challenge for the patients to receive effective treatment in time. The brain-derived neurotrophic factor (BDNF) is the most abundant neurotrophin in the adult brain, which possesses a remarkable capability to repair brain damage. Recent promising preclinical outcomes have made BDNF a popular late-stage target in the development of novel stroke treatments. In this review, we aim to summarize the latest progress in the understanding of the cellular/molecular mechanisms underlying stroke pathogenesis, current strategies and difficulties in drug development, the mechanism of BDNF action in poststroke neurorehabilitation and neuroplasticity, and recent updates in novel therapeutic methods.

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Section: Bdnf As a Therapeutic Agent In The Treatment Of Strokementioning

confidence: 99%

Brain-Derived Neurotrophic Factor and Its Potential Therapeutic Role in Stroke Comorbidities

et al. 2020

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“…Studies showed that HSYA plays a protective role in animal models of pulmonary inflammatory injury [19, 20], cardiac failure [21, 22], and liver fibrosis [23, 24]. HSYA features extreme neuroprotection in animal models of acute and chronic central nervous system (CNS) injuries, including spinal cord ischemia, ischemia-reperfusion injury [17, 25, 26], and Parkinson’s disease [27]. Accumulated data suggest that HSYA can cure CNS lesions through mechanisms involving anti-inflammation and anti-oxidation.…”

Section: Introductionmentioning

confidence: 99%

HSYA alleviates secondary neuronal death through attenuating oxidative stress, inflammatory response, and neural apoptosis in SD rat spinal cord compression injury

Pei¹,

Fan²,

Nan³

et al. 2017

J Neuroinflammation

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BackgroundHydroxysafflor yellow A (HSYA) is a major active component of yellow pigment extracted from safflowers; this compound possesses potent neuroprotective effects both in vitro and in vivo. However, underlying mechanism of HSYA is not fully elucidated. The present study investigated the protective effects of HSYA in rat spinal cord compression injury model and related mechanisms involved.MethodsSprague–Dawley rats were divided as Sham, Control, and HSYA groups (n = 30 per group). Spinal cord injury (SCI) model was induced by application of vascular clips (force of 50 g, 1 min) to the dura at T9–T10 level of vertebra. Injured animals were administered with either HSYA (8 mg/kg at 1 and 6 h after injury, then 14 mg/kg, for a total of 7 days at 24-h time intervals) or equal volume of saline by intraperitoneal injection.ResultsFrom this experiment, we discovered that SCI in rats resulted in severe trauma, which is characterized by tissue damage, lipid peroxidation, neutrophil infiltration, inflammation mediator release, and neuronal apoptosis. However, HSYA treatment significantly reduced the following: (1) degree of tissue injury (histological score) and edema; (2) neutrophil infiltration (myeloperoxidase activity); (3) oxidative stress (superoxide dismutase, malondialdehyde, and nitric oxide); (4) pro-inflammatory cytokine expression (tumor necrosis factor-α, interleukin-6, inducible nitric oxide synthase, cyclooxygenase-2); (5) nuclear factor-κB activation; (6) apoptosis (terminal deoxynucleotidyl transferase dUTP nick end labeling staining and cysteine-aspartic protease-3 activity). Moreover, in a separate set of experiments, we clearly demonstrated that HSYA treatment significantly ameliorated recovery of limb function (as evaluated by Basso, Beattie, and Bresnahan behavioral recovery scores).ConclusionsTreatment with HSYA restrains development of oxidative stress, inflammation response, and apoptotic events associated with SCI of rats, demonstrating that HSYA is a potential neuroprotectant for human SCI therapy.

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“…As we all know, innate immune system activation plays an important role in cerebral ischemia reperfusion injury, and the attenuation of active proinflammatory molecules derived from innate immune system has become the focus of therapeutic strategy [20]. HP has anti-oxidation effect in the blood [9].…”

Section: Discussionmentioning

confidence: 99%

Elevated Plasma Haptoglobin Level as a Potential Marker for Poor Prognosis in Acute Cerebral Infarction

Zhang

Xiang

2018

Eur Neurol

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Background: Relationship between peripheral circulation concentration of haptoglobin (Hp) and risk of cerebrovascular disease has not been well investigated so far. The aim of the study was to reveal the prognostic significance of Hp on acute cerebral infarction. Methods: A total of 200 patients with acute cerebral infarction and 200 controls were included. Research data were collected from their medical records. Blood samples were obtained on admission. Hp phenotyping was performed using a native polyacrylamide gel electrophoresis. Plasma Hp levels were determined using enzyme-linked immunosorbent assays. The patients were followed up yearly, and endpoint was overall death. Results: Plasma levels of Hp were significantly elevated in the patients than in the controls (p < 0.001). Three-year overall death in the follow-up period was associated with the high plasma level of Hp (Hazard ratio [HR] 2.33, 95% CI 1.74–3.12). But, 3-year overall death was not related to Hp phenotyping (Hp 2–1 vs. 1–1: HR 1.07, 95% CI 0.66–1.73; Hp 2–2 vs. 1–1: HR 1.08, 95% CI 0.67–1.74). Conclusion: Peripheral circulation concentration of Hp might be an independent prognostic factor for acute cerebral infarction. But there was no relationship between Hp phenotyping and prognosis in this disease.

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Hydroxysafflor yellow A exerts neuroprotective effects in cerebral ischemia reperfusion-injured mice by suppressing the innate immune TLR4-inducing pathway

Cited by 53 publications

References 42 publications

Brain-Derived Neurotrophic Factor and Its Potential Therapeutic Role in Stroke Comorbidities

Brain-Derived Neurotrophic Factor and Its Potential Therapeutic Role in Stroke Comorbidities

HSYA alleviates secondary neuronal death through attenuating oxidative stress, inflammatory response, and neural apoptosis in SD rat spinal cord compression injury

Elevated Plasma Haptoglobin Level as a Potential Marker for Poor Prognosis in Acute Cerebral Infarction

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