Journal: Frontiers in Pharmacology

Article Title: Therapeutic effects of traditional Chinese medicine Hua-Feng-Dan in a rat model of ischemic stroke involve renormalization of gut microbiota

doi: 10.3389/fphar.2025.1485340

Figure Lengend Snippet: Hua-Feng-Dan ameliorates the size of the brain infarct and the neurological impairments. Animals were subjected to middle cerebral artery occlusion or sham surgery, then left untreated (MCAO, Sham) or treated with nimodipine (NMDP) or Hua-Feng-Dan at a low dose (HFD-L, 0.162 g/kg), intermediate dose (HFD-M, 0.324 g/kg) or high dose (HFD-H, 0.648 g/kg). (A) Representative photographs of ischemic halves of brains after TTC staining. (B) Extent of cerebral infarction (n = 3). (C) Brain water content (n = 4). (D) Neurological score (n = 20). Quantitative data are mean ± SD. *** P < 0.001 vs. Sham group; ## P < 0.01, ### P < 0.001 vs. MCAO group; based on one-way ANOVA and Tukey’s multiple-comparisons post hoc test.

Article Snippet: Rats were randomized to receive, by oral gavage, saline instead of drug treatment or one of the following drugs dissolved in saline: the calcium channel blocker nimodipine (NMDP, batch 211274, Yabao Pharmaceutical, Shanghai, China), which is widely used to ischemic cerebrovascular disease; and Hua-Feng-Dan.

Techniques: Staining

Journal: Frontiers in Pharmacology

Article Title: Therapeutic effects of traditional Chinese medicine Hua-Feng-Dan in a rat model of ischemic stroke involve renormalization of gut microbiota

doi: 10.3389/fphar.2025.1485340

Figure Lengend Snippet: Hua-Feng-Dan alleviates histopathology injury and apoptosis of nerve cells after ischemic stroke in rats. Animals were subjected to middle cerebral artery occlusion or sham surgery, then left untreated (MCAO, Sham) or treated with nimodipine (NMDP) or Hua-Feng-Dan at a low dose (HFD-L, 0.162 g/kg), intermediate dose (HFD-M, 0.324 g/kg) or high dose (HFD-H, 0.648 g/kg). (A) Thin sections of brain tissue after hematoxylin-eosin staining (n = 3). Blue arrows represent macrophage infiltration or vascular stasis; red arrows, necrotic neurons or pyramidal cells; green arrows, glial cell proliferation; yellow arrows, vacuoles or septa; and black arrows, crumpled neurons or pyramidal cells. Scale bar, 100 μm. (B) Thin sections of brain tissue after terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) staining (n = 3). Scale bar, 100 μm. (C) TUNEL positive cells density (n = 3).

Article Snippet: Rats were randomized to receive, by oral gavage, saline instead of drug treatment or one of the following drugs dissolved in saline: the calcium channel blocker nimodipine (NMDP, batch 211274, Yabao Pharmaceutical, Shanghai, China), which is widely used to ischemic cerebrovascular disease; and Hua-Feng-Dan.

Techniques: Histopathology, Staining, End Labeling, TUNEL Assay

Journal: Frontiers in Pharmacology

Article Title: Therapeutic effects of traditional Chinese medicine Hua-Feng-Dan in a rat model of ischemic stroke involve renormalization of gut microbiota

doi: 10.3389/fphar.2025.1485340

Figure Lengend Snippet: Hua-Feng-Dan restores the integrity of the intestinal barrier after ischemic stroke in rats. Animals were subjected to middle cerebral artery occlusion or sham surgery, then left untreated (MCAO, Sham) or treated with a high dose of Hua-Feng-Dan (HFD, 0.648 g/kg) and nimodipine (NMDP). (A) Representative photographs of colon H&E staining (n = 3). Red arrows indicate the presence of lymphocytic infiltration; blue arrows, edema or edematous mucosal epithelial cells; black arrows, necrosis of mucosal epithelial cells; yellow arrows, dilated intestinal glands; and purple arrows, vasodilation. Scale bar = 200 and 100 μm. (B–D) Comparison of levels of three indices of intestinal barrier permeability: lipopolysaccharide (LPS), diamine oxidase (DAO) and d -lactate ( d -LA). (E–G) Comparison of levels of three pro-inflammatory factors: tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. (H) Comparison of levels of total cholesterol (T-CHO) as an index of dyslipidemia. (I, J) Comparison of levels of oxidative stress factors total superoxide dismutase (T-SOD) and malondialdehyde (MDA). Data are mean ± SD, n = 6 (excluding H&E staining). * P < 0.05, ** P < 0.01, *** P < 0.001 vs. Sham group; # P < 0.05, ## P < 0.01, ### P < 0.001 vs. MCAO group (based on one-way ANOVA and Tukey’s multiple-comparisons post hoc test).

Article Snippet: Rats were randomized to receive, by oral gavage, saline instead of drug treatment or one of the following drugs dissolved in saline: the calcium channel blocker nimodipine (NMDP, batch 211274, Yabao Pharmaceutical, Shanghai, China), which is widely used to ischemic cerebrovascular disease; and Hua-Feng-Dan.

Techniques: Staining, Comparison, Permeability

Journal: Frontiers in Neuroscience

Article Title: GluN2A/ERK/CREB Signaling Pathway Involved in Electroacupuncture Regulating Hypothalamic-Pituitary-Adrenal Axis Hyperactivity

doi: 10.3389/fnins.2021.703044

Figure Lengend Snippet: The GluN2A, ERK, and CREB antagonist reverses HPA axis hyperactivity induced by surgery. The GluN2A antagonist PEAQX (1 μg/μL, 0.25 μL/side) was administered to both sides of the hypothalamus. Hypothalamus was dissected 24 h after the PEAQX administration. (A–D) Representative bands and quantification of hypothalamic pERK, pCREB, and CRH protein among the NS, HT + NS, HT + PEAQX, and HT + EA groups ( n = 4 for each group). The ERK inhibitor MEK1/2 Inhibitor IV (0.1 nmol/μL, 0.5 μL/side) was administered stereotaxically into the hypothalamus. (E–G) Representative bands and quantification of pCREB and CRH protein in the NS, HT + NS, HT + MEK, and HT + EA groups ( n = 5 for each group). 666-15 (an antagonist of CREB, 0.1 nmol/μL, 0.5 μL/side) was administrated to investigate the relationship between CREB and HPA axis. (H,I) Western Blot analysis of hypothalamic CRH protein in the NS, HT + NS, HT + 666-15, and HT + EA groups ( n = 5 for each group). (J) Relative hypothalamic CRH mRNA expression after surgical trauma and drugs administration ( n = 5 for each group). (K,L) ACTH and CORT levels in the peripheral serum of mice ( n = 5 for each group). Data are expressed as mean ± SEM. *vs. NS group (* p < 0.05, ** p < 0.01, *** p < 0.001); #vs. HT group ( # p < 0.05, ## p < 0.01, ### p < 0.001).

Article Snippet: The separated groups of mice were administrated NMDA (M3262, Sigma, United States; an agonist of GluN2A-containing NMDA receptors, 0.4 nmol/μL, 0.5 μL/side) , PEAQX (HY-12294A, Med Chem Express, China; a preferential antagonist of GluN2A-containing NMDA receptors, 1 μg/μL, 0.25 μL/side) , MEK1/2 Inhibitor IV (444967, Sigma, United States; an inhibitor of ERK, 0.1 nmol/μL, 0.5 μL/side) , 666-15 (HY-101120, Med Chem Express, China; an antagonist of CREB, 0.1 nmol/μL, 0.5 μL/side) , or normal saline into the bilateral hypothalamus (4–6 animals in each group) for functional research.

Techniques: Western Blot, Expressing

Journal: The Journal of Neuroscience

Article Title: Granule Neuron Regulation of Purkinje Cell Development: Striking a Balance Between Neurotrophin and Glutamate Signaling

doi: 10.1523/jneurosci.18-10-03563.1998

Figure Lengend Snippet: Figure 5. CNQX, but not APV, rescues Purkinje cells from BDNF toxicity. A, Experiments with CNQX; B, experiments with APV. Purified Purkinje and granule cells were cocultured in serum-free medium for 6 or 14 div, with or without 10 ng/ml BDNF, 50 mM APV (an NMDA receptor antagonist), or 50 mM CNQX (a non-NMDA receptor antagonist). Pur- kinje cell survival is represented as a percentage of the Purkinje cell number in untreated control cultures at each time point. Error bars indicate SE. div, Days in vitro. Asterisks, Statistically significant differences from BDNF-treated cultures; **p, , 0.01.

Article Snippet: The NMDA receptor antagonist D-APV and the non-NMDA receptor antagonist CNQX were purchased from Tocris Cookson and used at 50 mM.

Techniques: Control, In Vitro