Breast cancer therapy has always been a hard but urgent issue. Disruption of mitochondrial Ca2+ homeostasis has been reported as an effective antitumor strategy, while how to contribute to mitochondrial Ca2+ overload effectively is a critical issue. To solve this issue, we designed and engineered a dual enhanced Ca2+ nanogenerator (DECaNG), which can induce elevation of intracellular Ca2+ through the following three ways: Calcium phosphate (CaP)-doped hollow mesoporous copper sulfide was the basic Ca2+ nanogenerator to generate Ca2+ directly and persistently in the lysosomes (low pH). Near-infrared light radiation (NIR, such as 808 nm laser) can accelerate Ca2+ generation from the basic Ca2+ nanogenerator by disturbing the crystal lattice of hollow mesoporous copper sulfide via NIR-induced heat. Curcumin can facilitate Ca2+ release from the endoplasmic reticulum to cytoplasm and inhibit expelling of Ca2+ in cytoplasm through the cytoplasmic membrane. The in vitro study showed that DECaNG could produce a l...

Enhanced Intracellular Ca2+ Nanogenerator for Tumor-Specific Synergistic Therapy via Disruption of Mitochondrial Ca2+ Homeostasis and Photothermal Therapy

Therapeutic targets of neuroprotection and neurorestoration in ischemic stroke: Applications for natural compounds from medicinal herbs.

Structural diversity, bioactivities, and biosynthesis of natural diterpenoid alkaloids

A review of traditional and current methods used to potentially reduce toxicity of Aconitum roots in Traditional Chinese Medicine.

Metal ions influx is a double edged sword for the pathogenesis of Alzheimer's disease.

Abstract Context Folium Ginkgo extract and tetramethylpyrazine sodium chloride injection (Xingxiong injection) is a compound preparation commonly used for treating cerebral ischaemia/reperfusion injury in ischaemic stroke in China. However, its potential mechanisms on ischaemic stroke remain unknown. Objective This study explores the potential mechanisms of Xingxiong injection in vivo or in vitro. Materials and methods Sprague-Dawley (SD) rats were randomly assigned to five groups: the sham (normal saline), the model (normal saline) and the Xingxiong injection groups (12.5, 25 or 50 mL/kg). The rats were subjected to 2 h of middle cerebral artery occlusion (MCAO) followed by reperfusion for 14 d. Xingxiong injection was administered via intraperitoneal (i.p.) injection immediately after ischaemia induction for 14 d. Afterwards, rats were sacrificed at 14 d induced by administration of Xingxiong injection. Results Xingxiong injection significantly reduces infarct volume (23%) and neurological deficit scores (93%) compared with the MCAO/R group. Additionally, Xingxiong injection inhibits the loss in mitochondrial membrane potential (43%) and reduces caspase-3 level (44%), decreases NOX (41%), protein carbonyl (29%), 4-HNE (40%) and 8-OhdG (41%) levels, inhibits the expression of inflammatory factors, such as TNF-α (26%), IL-1β (34%), IL-6 (39%), MCP-1 (36%), CD11a (41%) and ICAM-1 (43%). Moreover, Xingxiong injection can increase p-Akt/Akt (35%) and Nrf2 (47%) protein expression and inhibit NLRP3 (42%) protein expression. Conclusions Xingxiong injection prevents cerebral ischaemia/reperfusion injury via activating the Akt/Nrf2 pathway and inhibiting NLRP3 inflammasome. These findings provide experimental evidence for clinical use of drugs in the treatment of ischaemic stroke.

https://www.tandfonline.com/doi/pdf/10.1080/13880209.2021.2014895?needAccess=true

Folium Ginkgo extract and tetramethylpyrazine sodium chloride injection (Xingxiong injection) protects against focal cerebral ischaemia/reperfusion injury via activating the Akt/Nrf2 pathway and inhibiting NLRP3 inflammasome activation

Aconitine-induced Ca2+ overload causes arrhythmia and triggers apoptosis through p38 MAPK signaling pathway in rats.

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Folium Ginkgo extract and tetramethylpyrazine sodium chloride injection (Xingxiong injection) protects against focal cerebral ischaemia/reperfusion injury via activating the Akt/Nrf2 pathway and inhibiting NLRP3 inflammasome activation

Aconitine-induced Ca2+ overload causes arrhythmia and triggers apoptosis through p38 MAPK signaling pathway in rats.