Formononetin has been demonstrated to protect against cerebral ischemia-reperfusion injury, however its mechanism has to be further researched. This study examined the effect of formononetin on cerebral ischemia-reperfusion injury in rats using the PARP-1/PARG/Iduna signaling pathway. In male SD rats, a model of cerebral ischemia-reperfusion injury was developed. Animals were randomly assigned to one of eight groups: Sham operation, Sham operation + formononetin, MCAO, MCAO + formononetin, PARP inhibitor (PJ34) + MCAO, formononetin + PJ34 + MCAO, PARG inhibitor (Ethacridine lactate) + MCAO, and ethacridine lactate + formononetin. The neurological deficit test, TTC staining, HE staining, Nissl staining, TUNEL staining, and western blotting were utilized to assess formononetin's protective effects in MCAO rats. The data show that formononetin can effectively alleviate neurological dysfunction and pathological changes in brain tissue in rats with cerebral ischemia-reperfusion injury, reduce the area of cerebral infarction and neuronal apoptosis, decrease the protein levels of PARP-1, PARG, Caspase-3, P53, and AIF in brain tissue, and increase the protein levels of Iduna and p-AKT. As a result, we concluded that formononetin improves brain ischemia-reperfusion injury in rats by modulating the PARP-1/PARG/Iduna signaling pathway.

Rationale: Anticoagulant rodenticides (ARs) are a substantial fraction of murine types. AR poisoning causes bleeding from the skin, mucous membranes, and multiple organs. However, reports of AR-induced cerebral hemorrhage are scarce. Patient concerns: A 40-year-old male presented with dizziness, headache, and limb weakness for 5 days and with coagulopathy. Two days prior to the onset of these symptoms, the patient was exposed to dead mice. Diagnoses: Rodenticide intoxication-induced cerebral hemorrhage. Interventions: Vitamin K1 infusion, administration of dehydrating agents to reduce intracranial pressure, and correction of acid-base and electrolyte imbalances. Outcomes: After 9 days of treatment, the patient’s symptoms were relieved, and reexamination revealed that coagulation parameters returned to normal levels. The patient was eventually discharged for observation with oral vitamin K1. Conclusions: Rodenticide poisoning can lead to intracerebral hemorrhage, and treatment with vitamin K1 infusion is effective. Lesson: Rodenticide poisoning-induced cerebral hemorrhage is rarely reported. Because its symptoms are nonspecific, it is easy to miss the diagnosis or misdiagnose. When patients present with direct and indirect symptoms such as dizziness, headache, and limb weakness, rodenticide poisoning should be considered. Coagulation function and head computed tomography or magnetic resonance imaging examination should be performed at the earliest to confirm the diagnosis and provide timely treatment.

This study aimed to investigate the effects of Miao medicinal Canna edulis RS3-resistant starch on behavioral performance and substantia nigra neuron apoptosis-related indicators in a rat model of Parkinson's disease (PD). Among the experimental groups, except for the control group, we induced PD rat models by subcutaneous injection of rotenone in the neck and back. After model induction, a 28-day drug intervention was conducted. Various techniques have been employed, including behavioral analysis, Real-time Polymerase Chain Reaction (RT-PCR), western blotting, enzyme-linked immunosorbent assay (ELISA), immunofluorescence, and terminal deoxynucleotidyltransferase-mediated UTP nick-ends. labeling (TUNEL) and Nissl staining to investigate the effect of Canna edulis RS3-resistant starch on the substantia nigra and neuronal apoptosis-related markers in the brains of PD model rats. Our study revealed that Canna edulis RS3, a resistant starch, significantly reduced the climbing time of PD model rats, prolonged their hanging time, lowered the expression levels of the inflammatory factors IL-1β, IL-6, and TNF-α, increased the number of TH-positive neurons in the substantia nigra, and decreased the levels of IL-1β, IL-6, and TNF-α. Furthermore, Canna edulis RS3 elevated the protein expression levels of tyrosine hydroxylase (TH) and Bcl-2 while reducing those of Bax, TLR4, NLRP3,and p-P65, and mitigated apoptosis and morphological changes in dopaminergic neurons in the substantia nigra region. Our results suggest that Canna edulis RS3-resistant starch may offer therapeutic benefits for PD patients with PD by potentially influencing inflammation and apoptosis in the dopaminergic system.

Introduction: Vascular dementia (VaD) is closely associated with oxidative stress and intracellular calcium overload. PLCγ1, IP3R, CAMKKII, and CaM proteins play important roles in mediating intracellular calcium overload and excessive accumulation of reactive oxygen species (ROS). Tongqiao Huashuan (TQHS) granules represent a formulated preparation derived from traditional Chinese medicine (TCM), which have demonstrated extensive clinical application in managing VaD. Although TQHS granules have shown favorable clinical efficacy, the underlying mechanisms remain unclear. The present investigation sought to clarify protective roles exerted by TQHS granules against VaD via modulation of relevant signaling cascades. Methods: Using a permanent bilateral common carotid artery occlusion (2-VO) rat model and an OGD/R-induced SH-SY5Y cell model, we evaluated cognitive function, neuronal injury, and pathway-related molecular changes. Results: TQHS granules markedly ameliorated behavioral deficits and restored cognitive performance in VaD rats following treatment. Immunohistochemistry and Western blotting experiments demonstrated that TQHS granules regulated protein abundance of PLCγ1, p-PLCγ1, IP3R, CAMKKII, and CaM, which are proteins related to the PLCγ1/IP3R signaling pathway, in vivo . Data derived from CCK-8, microplate reader detection, and immunofluorescence experiments demonstrated that TQHS granules increased cell survival rate, reduced intracellular Ca ²⁺ concentration, and reduced ROS levels. RT-qPCR showed that TQHS granules increased the expression of PLCγ1, IP3R and TrkB. Discussion: The neuroprotective effect of TQHS granules on experimental VaD may be mediated by regulating the PLCγ1/IP3R pathway, improving oxidative stress injury and intracellular calcium overload in VaD. TQHS granules hold considerable promise as a viable complementary intervention capable of retarding the neurodegenerative trajectory of VaD.

Age-related declines in visual and auditory function are closely linked to cognitive deterioration in older adults. While cross-modal audiovisual training has shown potential for enhancing perceptual sensitivity, its underlying neural mechanisms and transfer effects on higher-order cognitive functions remain largely underexplored. This study aimed to investigate the effects of adaptive audiovisual perceptual training (APT) on cognitive performance and neural activation in older adults. Ninety-two older adults (mean age = 66.3 years, range = 60-77) were assigned to a training group (TG; n = 47) or a control group (CG; n = 45). The TG completed a 7-day APT program, while the CG received no intervention. All participants underwent pretest and posttest assessments, including a training task, audiovisual discrimination task, attention network test (ANT), and audiovisual associative 2-back. Training led to significant behavioral improvements in the TG, as reflected by higher accuracy and faster responses. At the neural level, the TG exhibited enhanced P3 amplitudes over parietal region in the training task, increased P3-AVI amplitudes over central and centro-parietal regions in the audiovisual discrimination task, greater P3 amplitudes over parietal region in the ANT, and increased P2 amplitudes over frontal, fronto-central, and central regions in the 2-back task. These findings demonstrate that adaptive APT effectively enhances audiovisual integration, attentional processing, and working memory in older adults. The results highlight its potential as a non-pharmacological intervention for mitigating age-related cognitive decline.