Acute myocardial infarction is an ischemic injury of the myocardium caused by an imbalance in the blood supply to myocardial tissues, which poses a serious threat to human life and health. Oxidative stress has been recognized as a significant contributor to acute myocardial infarction. Salvia miltiorrhiza Carbonisata (SMC) is among the most frequently employed herbal remedies for the treatment of acute myocardial infarction; however, the exact identity of its principal active constituents is not well defined. Research indicates that carbon dots (CDs) exhibit significant biological properties. Consequently, we initially synthesized carbon dots (CDs) from Salvia miltiorrhiza Carbonisata, with the objective of exploring how SMC-CDs mitigate isoproterenol (ISO)-induced myocardial infarction (MI) in rats. The results showed that the pretreatment with SMC-CDs markedly enhanced compromised cardiac function, mitigated myocardial fibrosis and the infiltration of inflammatory cells, decreased the size of the infarct, and suppressed cardiomyocyte apoptosis. Furthermore, the antioxidant properties of myocardial tissue were enhanced, and oxidative stress caused by free radicals was effectively mitigated by SMC-CDs, which succeeded in reducing levels of myocardial enzymes and elevating the activity of relevant ATPases. This implies that SMC-CDs could be a potential candidate for novel nanomedicine strategies designed to address cardiovascular ailments.

Background: Temporal lobe epilepsy (TLE), a prevalent refractory focal epilepsy frequently complicated by comorbid anxiety and depression, poses significant therapeutic challenges due to the inadequate efficacy of current antiepileptic drugs in seizure control. Carbon dots (CDs) demonstrate notable biological activities and represent a promising class of nanomedicines for TLE intervention. Methods: This study established an eco-friendly calcination protocol to synthesize a novel suspension of Crinis Carbonisatus-derived carbon dots (CC-CDs) as a candidate therapeutic for TLE. Results: In a TLE mouse model, the CC-CDs suspension significantly inhibited phosphorylation of the MAPK pathway (p-JNK, p-ERK, p-p38; p < 0.01, p < 0.05), leading to reduced levels of pro-inflammatory cytokines (IL-6, IL-1β, TNF-α; p < 0.01, p < 0.05), upregulation of TGF-β1 (p < 0.01, p < 0.05), and restoration of antioxidant enzyme activities (SOD, GSH, CAT; p < 0.01, p < 0.05). These modifications subsequently regulated the Glu/GABA balance, alleviating excitotoxicity (p < 0.05), attenuating neuronal damage and Nissl body loss in hippocampal CA1/CA3 regions, and improving cognitive function alongside reducing anxiety-like behaviors (p < 0.01, p < 0.05). In vitro, the CC-CDs suspension suppressed LPS-induced apoptosis in BV2 cells. Conclusions: The CC-CDs suspension ameliorates TLE by inhibiting MAPK signaling, thereby reducing neuroinflammation and oxidative stress, rectifying Glu/GABA imbalance, attenuating excitotoxicity, and ultimately improving behavioral deficits. These findings underscore the therapeutic potential of CC-CDs suspension for TLE treatment.