Neuroprotective effects of osthole pretreatment against traumatic brain injury in rats

He, Yalong; Qu, Shuoyao; Wang, Jiang; He, Xiaosheng; Wang, Lin; Zhen, Hai‐Ning; Zhang, Xiang

doi:10.1016/j.brainres.2011.11.027

Cited by 61 publications

(33 citation statements)

References 46 publications

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“…Osthole decreased oxidative stress, indicating potential antioxidant effects of osthole, as reported previously. 33 During ischemia-reperfusion, the ischemic tissue and remote organs release inflammatory cytokines such as TNF-α and IL-1β, inflammatory cells accumulate, and intestinal inflammatory damage occurs. 34 The cytokine IL-1β can induce and promote damage by inflammatory mediators, edema formation, and various pathologic processes.…”

Section: Discussionmentioning

confidence: 99%

Untitled

2014

Exp Clin Transplant

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Objectives: The purpose of this study was to evaluate the effect of intravenous injection of osthole on intestinal ischemia-reperfusion injury and parameters of oxidative stress. Materials and Methods: In 45 Kunming male mice, treatment included sham surgery (15 mice); intestinal ischemia-reperfusion injury (clamping of the superior mesenteric artery, 2 h; clamp release, 1 h; 15 mice); or osthole treatment before and after ischemia-reperfusion injury (15 mice). Evaluation included histopathology, determination of intestinal wet/dry weight ratio, and measurement of levels of diamine oxidase, superoxide dismutase, malondialdehyde, interleukin 1β, tumor necrosis factor α, and interleukin 2. Intestinal barrier permeability was evaluated with Evans blue test. Results: The mean wet-to-dry weight ratio, Evans blue content, and Chiu score were significantly greater in the ischemia-reperfusion than in the sham group and lower in the osthole-treated than the ischemia-reperfusion group. The mean serum diamine oxidase, malondialdehyde, interleukin 1β, and tumor necrosis factor α levels were significantly greater in the ischemia-reperfusion than in the sham group and lower in the osthole-treated than in the ischemia-reperfusion group. The mean superoxide dismutase activity and interleukin 2 levels were lower in the ischemia-reperfusion than in the sham group and greater in the osthole-treated than in the ischemia-reperfusion group. Conclusions: Treatment with osthole may protect against oxidative stress and tissue damage from intestinal ischemia-reperfusion injury.

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Section: Discussionmentioning

confidence: 99%

Untitled

2014

Exp Clin Transplant

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“…Osthole, isolated from the TCM Cnidium monnieri, was found to reduce neurological deficits, cerebral edema, and hippocampal neuron loss by inhibiting mitochondria- BT: body temperature; ICP: intracranial pressure; HITDT: hemorrhage in the digestive tract; S100B: S100 calcium-binding protein beta; NSE: neuron-specifi c enolase; VEGF: vascular endothelial growth factor; NGF: nerve growth factor; GDNF: glial cell line-derived neurotrophic factor; NCAM: neural cell adhesion molecule; NSC: neural stem/progenitor cell; HSP70: 70 kilodalton heat shock proteins; SOD: superoxide dismutase. mediated signaling pathways and inhibiting ROS release in rats (108). Curculigoside, a component of Curculigo orchioides Gaertn., was found to reduce neuronal cell loss by blocking mitochondria-mediated signaling pathways and inhibiting ROS production in cortex neurons (109).…”

Section: Alternative and Complementary Medicinementioning

confidence: 99%

Advances in diagnosis, treatments, and molecular mechanistic studies of traumatic brain injury

Xia

Wang

et al. 2015

BST

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“…[5][6][7][8][9] Ost has various pharmacological and biological applications, and current research is focused on its antitumor activity. Several previous studies have reported that Ost is effective in inducing cell apoptosis, arresting cell cycle, and inhibiting cell proliferation.…”

Section: Introductionmentioning

confidence: 99%

N-Succinyl-chitosan nanoparticles coupled with low-density lipoprotein for targeted osthole-loaded delivery to low-density lipoprotein receptor-rich tumors

Zhang¹,

Zhu²,

Zhou³

et al. 2014

IJN

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N-Succinyl-chitosan (NSC) was synthesized and NSC nanoparticles (NPs) with loaded osthole (Ost) (Ost/NSC-NPs) were prepared by emulsion solvent diffusion. Subsequently, low-density lipoprotein (LDL)-mediated NSC-NPs with loaded Ost (Ost/LDL-NSC-NPs) were obtained by coupling LDL with Ost/NSC-NPs through amide linkage. The average particle size of Ost/NSC-NPs was approximately 145 nm, the entrapment efficiency was 78.28%±2.06%, and the drug-loading amount was 18.09%±0.17%. The release of Ost from Ost/NSC-NPs in vitro showed a more evident sustained effect than the native material. The half maximal inhibitory concentration of Ost/LDL-NSC-NPs was only 16.23% that of the free Ost at 24 hours in HepG2 cells. Ost inhibited HepG2 cell proliferation by arresting cells in the synthesis phase of the cell cycle and by triggering apoptosis. Cellular uptake and subcellular localization in vitro and near-infrared fluorescence real-time imaging in vivo showed that Ost/LDL-NSC-NPs had high targeting efficacy. Therefore, LDL-NSC-NPs are a promising system for targeted Ost delivery to liver tumor.

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Neuroprotective effects of osthole pretreatment against traumatic brain injury in rats

Cited by 61 publications

References 46 publications

Untitled

Untitled

Advances in diagnosis, treatments, and molecular mechanistic studies of traumatic brain injury

N-Succinyl-chitosan nanoparticles coupled with low-density lipoprotein for targeted osthole-loaded delivery to low-density lipoprotein receptor-rich tumors

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