Brain-wide mapping of c-Fos expression in nitroglycerin-induced models of migraine.

BACKGROUND: Migraine is a neurological disorder characterized by complex, widespread, and sudden attacks with an unclear pathogenesis, particularly in chronic migraine (CM). Specific brain regions, including the insula, amygdala, thalamus, and cingulate, medial prefrontal, and anterior cingulate cortex, are commonly activated by pain stimuli in patients with CM and animal models. This study employs fluorescence microscopy optical sectioning tomography (fMOST) technology and AAV-PHP.eB whole-brain expression to map activation patterns of brain regions in CM mice, thus enhancing the understanding of CM pathogenesis and suggesting potential treatment targets. METHODS: By repeatedly administering nitroglycerin (NTG) to induce migraine-like pain in mice, a chronic migraine model (CMM) was established. Olcegepant (OLC) was then used as treatment and its effects on mechanical pain hypersensitivity and brain region activation were observed. All mice underwent mechanical withdrawal threshold, light-aversive, and elevated plus maze tests. Viral injections were administered to the mice one month prior to modelling, and brain samples were collected 2 h after the final NTG/vehicle control injection for whole-brain imaging using fMOST. RESULTS: In the NTG-induced CMM, mechanical pain threshold decreased, photophobia, and anxiety-like behavior were observed, and OLC was found to improve these manifestations. fMOST whole-brain imaging results suggest that the isocortex-cerebral cortex plate region, including somatomotor areas (MO), somatosensory areas (SS), and main olfactory bulb (MOB), appears to be the most sensitive area of activation in CM (P < 0.05). Other brain regions such as the inferior colliculus (IC) and intermediate reticular nucleus (IRN) were also exhibited significant activation (P < 0.05). The improvement in migraine-like symptoms observed with OLC treatment may be related to its effects on these brain regions, particularly SS, MO, ansiform lobule (AN), IC, spinal nucleus of the trigeminal, caudal part (Sp5c), IRN, and parvicellular reticular nucleus (PARN) (P < 0.05). CONCLUSIONS: fMOST whole-brain imaging reveals c-Fos + cells in numerous brain regions. OLC improves migraine-like symptoms by modulating brain activity in some brain regions. This study demonstrates the activation of the specific brain areas in NTG-induced CMM and suggests some regions as a potential treatment mechanism according to OLC.

Therapeutic effect of notoginseng saponins before and after fermentation on blood deficiency rats.

Notoginseng saponins (NS) are the active ingredients in Panax notoginseng (Burk.) F.H. Chen (PN). NS can be transformed depending on how the extract is processed. Fermentation has been shown to produce secondary ginsenosides with increased bioavailability. However, the therapeutic effect of fermented NS (FNS) requires further study. The present study compared the compositions and activities of FNS and NS in blood deficiency rats, which resembles the symptoms of anemia in modern medicine, induced by acetylphenylhydrazine and cyclophosphamide. A total of 32 rats were randomly divided into control, model, FNS and NS groups. A blood deficiency model was established and then treatment was orally administered for 21 days. The results of component analysis indicated that some saponins transformed during the fermentation process resulting in a decrease of notoginsenoside R1, and ginsenosides Rg1, Rb1 and Re, and an increase in ginsenosides Rd, Rh2, compound K, protopanaxadiol and protopanaxatriol. The animal results showed that both FNS and NS increased the number of white blood cells (WBCs), red blood cells, hemoglobin, platelets and reticulocytes, and the levels of granulocyte-macrophage colony-stimulating factor (GM-CSF), erythropoietin (EPO) and thrombopoietin (TPO), decreased the G0/G1 phase and increased G2/M phase, and decreased the apoptosis rate of bone marrow (BM) cells, which suggested a contribution to the recovery of hematopoietic function of the BM cells. FNS and NS increased the protein expression levels of the cytokines IL-4, IL-10, IL-12, IL-13, TGF-ß, IL-6, IFN-γ and TNF-α, and the mRNA expression levels of transcription factors GATA binding protein 3 and T-box expressed in T cell (T-bet). FNS and NS treatment also increased the number of CD4+ T cells, and decreased the enlargement of the rat spleen and thymus atrophy, which indicated a protective effect on the organs of the immune system. The results of the present study demonstrated that compared with NS, FNS showed an improved ability to increase the levels of WBCs, lymphocytes, GM-CSF, EPO, TPO, aspartate aminotransferase, IL-10, IL-12, IL-13 and TNF-α, and the mRNA expression levels of T-bet, and decrease alanine aminotransferase levels. The differences seen for FNS treatment could arise from their improved bioavailability compared with NS, due to the larger proportion of hydrophobic ginsenosides produced during fermentation.

Effect of corneal stiffness decrease on axial length elongation in myopia determined based on a mathematical estimation model.

Purpose: To investigate the relationship between the corneal material stiffness parameter stress-strain index (SSI) and axial length (AL) elongation with varying severities of myopia, based on a mathematical estimation model. Methods: This single-center, cross-sectional study included data from healthy subjects and patients preparing for refractive surgery in the Qingdao Eye Hospital of Shandong First Medical University. Data were collected from July 2021 to April 2022. First, we performed and tested an estimated AL model ( A L M o r g a n ) based on the mathematical equation proposed by Morgan. Second, we proposed an axial increment model ( Δ A L ) corresponding to spherical equivalent error (SER) based on A L e m m e t r o p i a ( A L M o r g a n at SER = 0) and subject's real AL. Finally, we evaluated the variations of Δ A L with SSI changes based on the mathematical estimation model. Results: We found that AL was closely associated with A L M o r g a n (r = 0.91, t = 33.8, p < 0.001) with good consistency and SER was negatively associated with Δ A L (r = -0.89, t = -30.7, p < 0.001). The association of SSI with AL, A L e m m e t r o p i a , and Δ A L can be summarized using the following equations: A L = 27.7 - 2.04 × S S I , A L e m m e t r o p i a = 23.2 + 0.561 × S S I , and Δ A L = 4.52 - 2.6 × S S I . In adjusted models, SSI was negatively associated with AL (Model 1: ß = -2.01, p < 0.001) and Δ A L (Model 3: ß = -2.49, p < 0.001) but positively associated with A L e m m e t r o p i a (Model 2: ß = 0.48, p < 0.05). In addition, SSI was negatively associated with Δ A L among subjects with AL ≥ 26 mm (ß = -1.36, p = 0.02). Conclusion: AL increased with decreasing SSI in myopia.

Analysis of m6A modulator-mediated methylation modification patterns and the tumor microenvironment in lung adenocarcinoma.

Lung adenocarcinoma (LUAD) is the most common histological subtype of lung cancer. In the development and progression of LUAD, epigenetic aberration plays a crucial role. However, the function of RNA N6-methyladenosine (m6A) modifications in the LUAD progression is unknown. The m6A regulator modification patterns in 955 LUAD samples were analyzed comprehensively. Patterns were systematically correlated with the tumor microenvironment (TME) cell-infiltration characteristics. Using principal component analysis algorithms, the m6Ascore was generated to quantify m6A modification patterns in individual tumors. Then, their values for predicting prognoses and therapeutic response in LUAD patients were assessed. Three distinct m6A modification patterns in LUAD were identified. Among them, the prognosis of m6Acluster C was the best, while the prognosis of m6Acluster A was the worst. Interestingly, the characterization of TME cell infiltration and biological behavior differed among the three patterns. To evaluate m6A modification patterns within individual tumors, an m6Ascore signature was constructed. The results showed that the high m6Ascore group was associated with a better prognosis; tumor somatic mutations and tumor microenvironment differed significantly between the high- and low- m6Ascore groups. Furthermore, in the cohort with anti-CTLA-4 treatment alone, patients with a high m6Ascore had higher ICI scores, which indicated significant therapeutic advantage and clinical benefits.

Hemostatic Effect of 20(S)-Panaxadiol by Induced Platelet Aggregation Depending on Calcium Signaling Pathway.

Panax notoginseng (Burk.) F.H. Chen is the most traditional hemostatic herb in China. Our previous research found that 20(S)-protopanaxadiol showed the hemostatic effect. And 20(S)-panaxadiol (PD) has a similar structure to 20(S)-protopanaxadiol with a dammarane skeleton. So, this article mainly studies the hemostatic effect of PD. The mouse tail amputation and liver scratch models were used to detect the hemostatic effect of PD. Blood routine and plasma coagulation parameters were measured by using a blood analyzer. The platelet aggregometer analyzed the platelet aggregation rate and adenosine triphosphate (ATP) concentration. Moreover, the intracellular calcium concentration ([Ca2+] i ), P-selectin (CD62P), PAC-1 (GP IIb/IIIa receptor marker), and cyclic adenosine monophosphate (cAMP) of platelets were also detected. The results showed that PD obviously shortened the bleeding time of the model mouse, affected the RBC and PLT parameters of rats, reduced APTT and TT, elevated FIB concentration, and promoted human/rat-washed platelet aggregation in vitro. PD promoted the release of ATP and [Ca2+] i and slightly increased the expression of CD62P and PAC-1 of platelets without 1 mM Ca2+. After adding 1 mM Ca2+, PD obviously increased ATP releasing and CD62P and GP IIb/IIIa expression rate and decreased the cAMP level of platelets. These parameter changes of PD-caused platelet were inhibited by vorapaxar. Besides, PD increased the phosphorylation of phosphoinositide 3-kinase/protein kinase B/glycogen synthase kinase 3ß (PI3K/Akt/GSK3ß) of human platelets. PD is an important hemostatic ingredient in Panax notoginseng, which induced platelet aggregation by affecting the calcium signaling and activating the PI3K/Akt/GSK3ß signaling pathway.

A randomised trial: effects of different anesthesia methods on early perioperative pain sensitivity and cellular immune function in patients undergoing radical mastectomy.

BACKGROUND: This study sought to investigate the effects of transversus thoracic muscle plane-pectoral nerves (TTP-PECS) block combined with propofol anesthesia on early perioperative pain sensitivity and cellular immune function in patients undergoing radical mastectomy. METHODS: A total of 115 patients who underwent radical mastectomy for breast cancer at our hospital from January 2019 to January 2021 were selected as the study subjects. The patients were allocated to the control group (n=57) or observation group (n=58) using a random number method. The control group was given simple general anesthesia, and the observation group was given TTP-PECS block combined with propofol anesthesia. The recovery time, pain [visual analogue scoring (VAS)] scores, and incidences of adverse reactions were compared between the 2 groups. Hemodynamic indicators [i.e., heart rate (HR), mean arterial pressure (MAP)], stress indicators [i.e., blood glucose (GLU), epinephrine (E), cortisol (Cor)], and the cellular immune function ofthe2 groups before anesthesia (T0), at the end of operation (T1), 1day after operation (T2) and 3days after operation (T3) were recorded. RESULTS: The spontaneous respiration recovery time, time to full wakefulness and the extubation time of the observation group were shorter than those of the control group (P<0.05). The observation group had lower VAS scores than the control group at 2, 8, 12, and 24 h after operation (P<0.05). The levels of MAP, HR, GLU, E and Cor in the observation group at T1, T2, and T3 were lower than those in the control group (P<0.05). Compared to the control group, the observation group had increased cluster of differentiation (CD)3+, CD4+, and CD4+/CD8+ cells (P<0.05), but there were no significant differences in CD8+ and natural killer (NK) cells between the 2 groups (P>0.05). The incidence of adverse reactions in the observation group was lower than that in the control group (8.62% vs. 24.56%) (P<0.05). CONCLUSIONS: TTP-PECS block combined with propofol anesthesia can relieve pain, shorten the recovery time, stabilize the hemodynamic level, and alleviate the stress responses of patients undergoing radical mastectomy with a slight suppression of cellular immune function and high safety. TRIAL REGISTRATION: Chinese Clinical Trial Registration Center ChiCTR2100048438.

Eukaryotic Translation Initiation Factor 3 Subunit B Is a Promoter in the Development and Progression of Pancreatic Cancer.

Background: Pancreatic cancer (PC) is a malignant tumor with hidden incidence, high degree of malignancy, rapid disease progression, and poor prognosis. Eukaryotic translation initiation factor 3 subunit B (EIF3B) is necessary for tumor growth, which is an alternative therapeutic target for many cancers. However, little is known about the relationship between EIF3B and PC. Methods: The expression of EIF3B in PC was detected by immunohistochemistry. EIF3B knockdown cell models were constructed by lentivirus infection. The MTT assay, the wound-healing assay, the transwell assay, the flow cytometry, and the Human Apoptosis Antibody Array was used to detect the effects of EIF3B knockdown on cell proliferation, cell migration, cell apoptosis, and cell cycle in vitro. Also, the effects of EIF3B knockdown on the tumor growth of PC were determined in vivo. Results: This study showed that the expression level of EIF3B was significantly up-regulated in PC tumor tissues and associated with pathological grade. In vitro, EIF3B knockdown inhibited the PC cell proliferation and migration, and the apoptosis levels were obviously promoted by regulating apoptosis-related proteins including Bcl-2, HSP27, HSP60, Survivin, sTNF-R2, TNF-α, TNF-ß, TRAILR-3, TRAILR-4, and XIAP. Furthermore, the tumor growth of PC was inhibited after the knockdown of EIF3B in vivo. Conclusion: EIF3B was up-regulated in PC and was a promoter in the development and progression of PC, which could be considered as a therapeutic target for the treatment of PC.

Clinical Features, Risk Factors, and Therapy of Epithelial Keratitis after Cataract Surgery.

PURPOSE: The study aimed to assess the clinical characteristics, risk factors, and therapy of epithelial keratitis after cataract surgery. METHODS: Medical data of 89 consecutive patients who developed epithelial keratitis after cataract surgery, including 37 patients with diabetes mellitus (37 eyes) and 52 patients without diabetes mellitus (52 eyes), were retrospectively reviewed. The clinical characteristics, risk factors, and therapy in those patients were evaluated. RESULTS: The preoperative tear film function determined by the tear breakup time, meibomian gland atrophy score, and low tear meniscus height in diabetic patients was poorer than nondiabetic patients (P < 0.001). Of diabetic patients, 83.78% (31/37) had been diagnosed with meibomian gland dysfunction before cataract surgery and treated with topical nonsteroidal anti-inflammatory drugs after cataract surgery for 44.69 ± 10.51 days, compared to 42.31% (22/52) of nondiabetic patients receiving the topical nonsteroidal anti-inflammatory treatment for 33.35 ± 5.16 days (both P < 0.001). Epithelial lesions progressed within three to four days following cataract surgery in 59.46% (22/37) of diabetic patients, versus 30.77% (16/52) of the nondiabetic patients (P=0.025). Patients with combined meibomian gland dysfunction and epithelial defects accounted for 48.65% (18/37) in the diabetic group and 25.00% (13/52) in the nondiabetic group (P < 0.001). In vivo confocal microscopy showed absence of subbasal never fibers in eyes with epithelial defects, and central corneal sensation was also significantly depressed in those eyes, but there was no significant difference between the two groups (P=0.227). Corneal ulceration and herpes simplex keratitis were found in 2.70% (1/37) and 5.41% (2/37) of diabetic patients, respectively. Amniotic membrane transplantation was required in 32.43% (12/37) of patients in the diabetic group, and the proportion was higher than 1.92% (1/52) in the nondiabetic group (P < 0.001). Average healing time of the corneal epithelium in the diabetic group was 40.62 ± 20.0 days, much longer than 21.74 ± 6.94 days in the nondiabetic group (P=0.002). CONCLUSION: Epithelial keratitis after cataract surgery in diabetic patients has the characteristics of rapid development, severe epithelial damage, and slow repair of the corneal epithelium. Amniotic membrane transplantation is a good choice for persistent epithelial defects associated with such epithelial keratitis. Attention should be paid to the tear film function and use of topical nonsteroidal anti-inflammatory drugs in patients undergoing cataract surgery.

Moscatilin Suppresses the Breast Cancer Both In Vitro and In Vivo by Inhibiting HDAC3.

Moscatilin, a natural compound isolated from the orchid Dendrobium moscatum, has multiple pharmacological actions. The present study investigated the anti-tumor role of moscatilin in breast cancer and elucidated the underlying mechanisms. Cell proliferation, viability, and apoptosis of moscatilin treated MDA-MB-231 cells were determined by CCK-8 assay and flow cytometry. Histone deacetylases (HDACs) expression levels and global acetylated status of breast cancer cells were detected by Western blot and qPCR. Mouse xenograft model was established to evaluate the anti-cancer effects of moscatilin. Moscatilin treatment dose dependently suppressed proliferation and increased apoptosis of breast cancer cells. Moreover, moscatilin administration dramatically repressed tumor growth and extended survival time of mouse model. Mechanistically, moscatilin down-regulated HDAC3 expression, and then enhanced the global acetylated status of histone H3 (H3K9Ac) and H4 (H4K16Ac). Our findings indicate that moscatilin can inhibit the proliferation and promote apoptosis of breast cancer in vitro and in vivo, which suggests that moscatilin can be used as a potential therapeutic agent for the treatment of breast cancer.

Integrated analysis of RNA-binding proteins in thyroid cancer.

Recently, the incidence of thyroid cancer (THCA) has been on the rise. RNA binding proteins (RBPs) and their abnormal expression are closely related to the emergence and pathogenesis of tumor diseases. In this study, we obtained gene expression data and corresponding clinical information from the TCGA database. A total of 162 aberrantly expressed RBPs were obtained, comprising 92 up-regulated and 70 down-regulated RBPs. Then, we performed a functional enrichment analysis and constructed a PPI network. Through univariate Cox regression analysis of key genes and found that NOLC1 (p = 0.036), RPS27L (p = 0.011), TDRD9 (p = 0.016), TDRD6 (p = 0.002), IFIT2 (p = 0.037), and IFIT3 (p = 0.02) were significantly related to the prognosis. Through the online website Kaplan-Meier plotter and multivariate Cox analysis, we identified 2 RBP-coding genes (RPS27L and IFIT3) to construct a predictive model in the entire TCGA dataset and then validate in two subsets. In-depth analysis revealed that the data gave by this model, the patient's high-risk score is very closely related to the overall survival rate difference (p = 0.038). Further, we investigated the correlation between the model and the clinic, and the results indicated that the high-risk was in the male group (p = 0.011) and the T3-4 group (p = 0.046) was associated with a poor prognosis. On the whole, the conclusions of our research this time can make it possible to find more insights into the research on the pathogenesis of THCA, this could be beneficial for individualized treatment and medical decision making.

Overexpressed WDR3 induces the activation of Hippo pathway by interacting with GATA4 in pancreatic cancer.

BACKGROUND: WD repeat domain 3 (WDR3) is involved in a variety of cellular processes including gene regulation, cell cycle progression, signal transduction and apoptosis. However, the biological role of WDR3 in pancreatic cancer and the associated mechanism remains unclear. We seek to explore the immune-independent functions and relevant mechanism for WDR3 in pancreatic cancer. METHODS: The GEPIA web tool was searched, and IHC assays were conducted to determine the mRNA and protein expression levels of WDR3 in pancreatic cancer patients. MTS, colony formation, and transwell assays were conducted to determine the biological role of WDR3 in human cancer. Western blot analysis, RT-qPCR, and immunohistochemistry were used to detect the expression of specific genes. An immunoprecipitation assay was used to explore protein-protein interactions. RESULTS: Our study proved that overexpressed WDR3 was correlated with poor survival in pancreatic cancer and that WDR3 silencing significantly inhibited the proliferation, invasion, and tumor growth of pancreatic cancer. Furthermore, WDR3 activated the Hippo signaling pathway by inducing yes association protein 1 (YAP1) expression, and the combination of WDR3 silencing and administration of the YAP1 inhibitor TED-347 had a synergistic inhibitory effect on the progression of pancreatic cancer. Finally, the upregulation of YAP1 expression induced by WDR3 was dependent on an interaction with GATA binding protein 4 (GATA4), the transcription factor of YAP1, which interaction induced the nuclear translocation of GATA4 in pancreatic cancer cells. CONCLUSIONS: We identified a novel mechanism by which WDR3 plays a critical role in promoting pancreatic cancer progression by activating the Hippo signaling pathway through the interaction with GATA4. Therefore, WDR3 is potentially a therapeutic target for pancreatic cancer treatment.

Elevation of miR-146a Inhibits BTG2/BAX Expression to Ameliorate Postoperative Cognitive Dysfunction Following Probiotics (VSL#3) Treatment.

It has been reported that the gut microbiome modulates postoperative cognitive dysfunction (POCD), and that administration of probiotics (VSL#3) may effectively relieve POCD. In this study, we aimed to identify the underlying mechanism of VSL#3 in POCD. A mouse model of POCD was constructed in adult male C57BL/6 mice, which were then treated with VSL#3. VSL#3 exerted a protective role against POCD and resultant neuronal apoptosis. The expression of miR-146a was found to be downregulated in hippocampal tissues of POCD mice, while VSL#3 could restore its expression. Loss- and gain-function approaches were conducted to determine the roles of microRNA (miR)-146a, B-cell translocation gene 2 (BTG2), and Bcl-2-associated X protein (Bax) in post-operative effects on cognitive function and neuronal apoptosis. The levels of reactive oxygen species (ROS), malondialdehyde (MDA), and superoxide dismutase (SOD) were measured to determine oxidative stress in brain tissue. The dual-luciferase reporter gene assay identified that miR-146a could target BTG2 and negatively regulate its expression. BTG2 knockdown suppressed neuronal apoptosis and contributed to shortened time of latency, prolonged time of mice spent in the target quadrant, and reduced oxidative stress through downregulating Bax expression. Finally, VSL#3 treatment upregulated the expression of miR-146a to block BTG2/Bax axis and consequently inhibited neuronal apoptosis and reduced oxidative stress in POCD mice. Taken together, the study suggested that miR-146a-mediated suppression of BTG2/Bax contributed to the protective role of probiotics treatment against POCD.

Impact of perioperative intravenous lidocaine infusion on postoperative pain and rapid recovery of patients undergoing gastrointestinal tumor surgery: a randomized, double-blind trial.

BACKGROUND: To explore the effect of perioperative intravenous lidocaine infusion on postoperative pain and the rapid recovery of patients undergoing gastrointestinal tumor surgery. METHODS: The patients who underwent gastrointestinal tumor surgery from May to July 2020 were selected. The patients were randomly divided into the lidocaine group (group L) and control group (group C) by the random number table method, with 60 patients in each group. Both groups of patients received an intravenous drug infusion immediately after induction of tracheal intubation under general anesthesia. In group L, 1.5 mg/kg lidocaine was slowly injected intravenously at a rate of 1.5 mg·kg-1·h-1 to the surgical suture, and intravenous inhalation was used to maintain the depth of anesthesia. Group C patients were given the same volume of normal saline. The 2-, 4-, 7-, 14-, 30-, and 90-day numerical rating scale (NRS) and the proportion of chronic post-surgical pain (CPSP) after 3 months for both groups after surgery were recorded. Each patient's postoperative comfort score, requiring analgesia, return of flatus, bowl movement, hospitalization days, hospitalization expenses, and adverse events were also recorded. RESULTS: One hundred and twenty patients were enrolled but 5 of them failed to complete the treatment process. Therefore, 58 and 57 patients in group L and C were included into the final analysis. The NRS of patients in group L was significantly lower than that of group C at all time points after surgery (P<0.05), and the proportion of CPSP in group L was significantly lower than that of group C (P<0.05). The percentage of patients requiring analgesia and postoperative comfort score of group L was significantly higher than that of group C (P<0.01), patient's return of flatus, bowl movement, hospitalization days, and hospitalization expenses in group L were significantly lower than those in group C (P<0.05). There were no difference of adverse events between the 2 groups (P>0.05). CONCLUSIONS: During the perioperative period of radical gastrointestinal tumor surgery, intravenous lidocaine infusion can reduce acute postoperative pain, promote postoperative gastrointestinal function recovery, and improve postoperative comfort.

Topiramate Reverses Physiological and Behavioral Alterations by Postoperative Cognitive Dysfunction in Rat Model Through Inhibiting TNF Signaling Pathway.

This study aimed to investigate the effects of topiramate (TPM) on rats with postoperative cognitive dysfunction (POCD) and elucidate the underlying mechanism. Differentially expressed genes in propofol-treated group and vehicle control group were filtered out and visualized in heatmap based on R program. POCD rat models were established for validation of TPM's anti-inflammatory action and Morris water maze (MWM) test was employed for assessment of spatial learning and memory ability of rats. Hematoxylin and eosin (HE) staining was applied to detect the neurodegeneration, and the apoptosis status was detected using TUNEL assay. In vitro, hippocampal microglia was treated with lipopolysaccharide or TPM to validate the TPM's anti-inflammatory action. Cell apoptosis was detected with flow cytometry. Inflammatory factors were detected by enzyme-linked immunosorbent assay, and factor-associated suicide (Fas), Fas-associated protein with death domain (FADD) expression were detected by western blot. As results, TPM administration improved the spatial learning and memory ability in POCD rat by decreasing the expression levels of Fas, FADD, and inflammatory factors (tumor necrosis factor-α, TNF-α; interleukin-1ß, IL-1ß; interleukin-6, IL-6) in POCD rats. In addition, TPM down-regulated cell apoptotic rate to suppress POCD by decreasing the expression of Caspase8, Bcl2-associated X (Bax), and poly ADP-ribose polymerase-1 (PARP1) yet enhancing B-cell lymphoma-2 (Bcl-2) expression. Besides, inhibition of Fas enhanced TPM-induced down-regulation of apoptosis of neuronal cell in hippocampus tissues of POCD rats. Our results revealed that treatment of POCD rats with TPM could suppress neuronal apoptosis in the hippocampus tissues, and the neuroprotective effects of TPM may relate with the regulation of tumor necrosis factor (TNF) signaling pathway.