Enhanced plasmonic scattering imaging via deep learning-based super-resolution reconstruction for exosome imaging.

Exosome analysis plays pivotal roles in various physiological and pathological processes. Plasmonic scattering microscopy (PSM) has proven to be an excellent label-free imaging platform for exosome detection. However, accurately detecting images scattered from exosomes remains a challenging task due to noise interference. Herein, we proposed an image processing strategy based on a new blind super-resolution deep learning neural network, named ESRGAN-SE, to improve the resolution of exosome PSI images. This model can obtain super-resolution reconstructed images without increasing experimental complexity. The trained model can directly generate high-resolution plasma scattering images from low-resolution images collected in experiments. The results of experiments involving the detection of light scattered by exosomes showed that the proposed super-resolution detection method has strong generalizability and robustness. Moreover, ESRGAN-SE achieved excellent results of 35.52036, 0.09081, and 8.13176 in terms of three reference-free image quality assessment metrics, respectively. These results show that the proposed network can effectively reduce image information loss, enhance mutual information between pixels, and decrease feature differentiation. And, the single-image SNR evaluation score of 3.93078 also showed that the distinction between the target and the background was significant. The suggested model lays the foundation for a potentially successful approach to imaging analysis. This approach has the potential to greatly improve the accuracy and efficiency of exosome analysis, leading to more accurate cancer diagnosis and potentially improving patient outcomes.

Molecular pharmacology and therapeutic advances of monoterpene perillyl alcohol.

BACKGROUND: Perillyl alcohol (POH) is a aroma monoterpene commonly obtained from various plants' essential oil. Recently, increasing researches have demonstrated that POH may be useful, not only as flavor compound, but also as bioactive molecule because of a variety of biological activities. PURPOSE: The aim of this review is to summarize the production, pharmacological activities and molecular mechanism, active derivatives, toxicity and parmacokinetics, and industrial application of POH. METHODS: A systematic search of published articles up to January 2024 in Web of Science, China Knowledge Network, and PubMed databases is conducted using the following keywords: POH, POH derivatives, biological or pharmacological, production or synthesis, pharmacokinetics, toxicity and application. RESULTS: Biotechnological production is considered to be a potential alternative approach to generate POH. POH provides diverse pharmacological benefits, including anticancer, antimicrobial, insecticidal, antioxidant, anti-inflammatory, hypotensive, vasorelaxant, antinociceptive, antiasthmatic, hepatoprotective effects, etc. The underlying mechanisms of action include modulation of NF-κB, JNK/c-Jun, Notch, Akt/mTOR, PI3K/Akt/eNOS, STAT3, Nrf2 and ERS response pathways, mitigation of mitochondrial dysfunction and membrane integrity damage, and inhibition of ROS accumulation, pro-inflammatory cytokines release and NLRP3 activation. What's more, the proteins or genes influenced by POH against diseases refer to Bax, Bcl-2, cyclin D1, CDK, p21, p53, HIF-1α, AP-1, caspase-3, M6P/IGF2R, PARP, VEGF, etc. Some clinical studies report that intranasal delivery of POH is a safe and effective treatment for cancer, but further clinical investigations are needed to confirm other health benefits of POH in human healthy. Depending on these health-promoting properties together with desirable flavor and safety, POH can be employed as dietary supplement, preservative and flavor additive in food and cosmetic fields, as building block in synthesis fields, as anticancer drug in medicinal fields, and as pesticides and herbicides in agricultural fields. CONCLUSION: This review systematically summarizes the recent advances in POH and highlights its therapeutic effects and potential mechanisms as well as the clinical settings, which is helpful to develop POH into functional food and new candidate drug for prevention and management of diseases. Future studies are needed to conduct more biological activity studies of POH and its derivatives, and check their clinical efficacy and potential side effects.

Universal and extensible language-vision models for organ segmentation and tumor detection from abdominal computed tomography.

The advancement of artificial intelligence (AI) for organ segmentation and tumor detection is propelled by the growing availability of computed tomography (CT) datasets with detailed, per-voxel annotations. However, these AI models often struggle with flexibility for partially annotated datasets and extensibility for new classes due to limitations in the one-hot encoding, architectural design, and learning scheme. To overcome these limitations, we propose a universal, extensible framework enabling a single model, termed Universal Model, to deal with multiple public datasets and adapt to new classes (e.g., organs/tumors). Firstly, we introduce a novel language-driven parameter generator that leverages language embeddings from large language models, enriching semantic encoding compared with one-hot encoding. Secondly, the conventional output layers are replaced with lightweight, class-specific heads, allowing Universal Model to simultaneously segment 25 organs and six types of tumors and ease the addition of new classes. We train our Universal Model on 3410 CT volumes assembled from 14 publicly available datasets and then test it on 6173 CT volumes from four external datasets. Universal Model achieves first place on six CT tasks in the Medical Segmentation Decathlon (MSD) public leaderboard and leading performance on the Beyond The Cranial Vault (BTCV) dataset. In summary, Universal Model exhibits remarkable computational efficiency (6× faster than other dataset-specific models), demonstrates strong generalization across different hospitals, transfers well to numerous downstream tasks, and more importantly, facilitates the extensibility to new classes while alleviating the catastrophic forgetting of previously learned classes. Codes, models, and datasets are available at https://github.com/ljwztc/CLIP-Driven-Universal-Model.

Hydrogen-Donor-Controlled Polybrominated Dibenzofuran (PBDF) Formation from Polybrominated Diphenyl Ether (PBDE) Photolysis in Solutions: Competition Mechanisms of Radical-Based Cyclization and Hydrogen Abstraction Reactions.

Polybrominated dibenzofurans (PBDFs) are characteristic dioxin-like products of polybrominated diphenyl ether (PBDE) photolysis. In this study, competition mechanisms of radical-based cyclization and hydrogen abstraction reactions are proposed in PBDF formation. Commonly, the ortho C-Br bond dissociation during photolysis generates aryl radicals, which undergo intramolecular cyclization to form PBDFs or hydrogen abstraction with hydrogen donors (such as organic solvents and water) to form lower brominated PBDEs. By using 2,4,4'-tribromodiphenyl ether (BDE-28) as the model reactant, the experimental PBDF formation ratios in various solutions are explained quantitatively by the calculated rate constants of cyclization and hydrogen abstraction reactions using the density functional theory (DFT) method. The solvent effect of pure and mixed solvents on PBDF formation is illustrated successfully. The structure-related hydrogen donation ability for hydrogen abstraction controls the bias of competition reactions and influences PBDF formation. Water resulted to be the most significant generation of PBDFs. Fulvic and humic acid display higher hydrogen donation ability than small-molecule organics due to the partitioning effect in aqueous solution. Quantitative structure-activity relationship (QSAR) models of the calculated rate constants for 512 cyclization and 319 hydrogen abstraction reactions using 189 PBDEs as the initial reactants in water are established, revealing the high risk of PBDF formation in aqueous solution.

Atorvastatin attenuates ferroptosis-dependent myocardial injury and inflammation following coronary microembolization via the Hif1a/Ptgs2 pathway.

Objectives: Coronary microembolization (CME) represents a serious periprocedural complication after percutaneous coronary intervention. Ferroptosis has been identified in multiple cardiovascular diseases. In this study, we aimed to investigate the effects of atorvastatin (ATV) on ferroptosis and inflammation following CME and elucidate the underlying mechanism. Methods: We established a rat model of CME by injecting microspheres into the left ventricle. Deferoxamine (DFO), a selective ferroptosis inhibitor, or ATV was pretreated before modeling. Cardiac function and cardiac troponin T (cTnT) levels were detected. Levels of ferroptosis-associated genes, malondialdehyde (MDA), glutathione (GSH), and ferrous iron (Fe2+) were measured to validate ferroptosis. Levels of tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1ß) were assayed to determine the inflammation. Chromatin immunoprecipitation was performed to determine the binding of hypoxia-inducible factor 1 subunit alpha (Hif1a) to the promoter of prostaglandin-endoperoxide synthase-2 (Ptgs2). Results: Ferroptosis and inflammation were induced following CME with increased levels of MDA (∼2.5 fold, p < 0.01), Fe2+ (∼1.5 fold, p < 0.01), TNF-α, and IL-1ß and decreased GSH levels (∼42%, p < 0.01). Meanwhile, the level of Ptgs2 was significantly increased, while those of glutathione peroxidase 4 (Gpx4) and solute carrier family 7 member 11 (Slc7a11) were decreased. The level of cTnT was increased by 7-fold (p < 0.01). Left ventricular ejection fraction (LVEF) was significantly reduced (∼85% in the sham group versus ∼45% in the CME group, p < 0.01). DFO or Ptgs2 silencing inhibited the increase of MDA, Ptgs2, TNF-α, and IL-1ß, and induced the levels of GSH and Gpx4, followed by reduction in cTnT levels by approximately 50% (p < 0.01). LVEF was improved by approximately 2 fold (p < 0.01). Mechanistically, the transcription factor Hif1a bound to the promoter of Ptgs2 and upregulated its expression. In addition, ATV inhibited the activation of the Hif1a/Ptgs2 axis and attenuated cardiac ferroptosis and inflammation, thus ameliorating CME-induced myocardial injury (LVEF, ∼34% elevation; cTnT, ∼1.8 fold decrease, p < 0.01). Conclusion: Atorvastatin ameliorates ferroptosis-mediated myocardial injury and inflammation following CME via the Hif1a/Ptgs2 pathway.

Nicorandil protects against coronary microembolization-induced myocardial injury by suppressing cardiomyocyte pyroptosis via the AMPK/TXNIP/NLRP3 signaling pathway.

BACKGROUND: Coronary microembolization (CME) is a common and intractable complication of coronary revascularization, which leads to perioperative myocardial injury, cardiac dysfunction, and poor prognosis. Nicorandil is widely used for the management of ischemic heart diseases, but the cardioprotective effects of nicorandil beyond anti-angina in CME-induced myocardial injury are worthy of further exploration. Therefore, the present study investigated the effect of nicorandil on CME-induced cardiomyocyte pyroptosis and explored the underlying mechanism. METHODS: A rat model of CME was established via the injection of microspheres into the left ventricle. A cell model of H9c2 cardiomyocytes stimulated by lipopolysaccharide (LPS) and hypoxia mimicked the microenvironment induced by CME. Nicorandil or the adenosine monophosphate-activated protein kinase (AMPK)-specific inhibitor compound C (CC) was administered before CME induction and cell modeling. Cardiac function, histological alterations in the myocardium, myocardial injury biomarkers in serum and cell culture supernatant, cell viability, adenosine triphosphate (ATP) level, superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, reactive oxygen species (ROS) activity, mitochondrial membrane potential, and pyroptosis-associated index were assessed after the animal and cell modeling of CME. RESULTS: Nicorandil pretreatment attenuated cardiac dysfunction and myocardial injury following CME. Nicorandil also alleviated oxidative stress and mitochondrial damage. Moreover, nicorandil promoted AMPK activation, reduced the expression of thioredoxin-interacting protein (TXNIP), inhibited the activation of the NOD-like receptor pyrin containing 3 (NLRP3) inflammasome, and mitigated cardiomyocyte pyroptosis. However, co-treatment with CC reversed the cardioprotective effects of nicorandil. CONCLUSION: Nicorandil pretreatment inhibits cardiomyocyte pyroptosis and alleviates CME-induced myocardial injury via the AMPK/TXNIP/NLRP3 signaling pathway.

Analysis of the Changes and Possible Reasons in Aberrations before and after Surgery in Patients with Concomitant Exotropia.

Objective: The objective is to observe the changes in aberrations before and after surgery in patients with common horizontal strabismus and to analyze the possible reasons for the changes. Methods: Forty eyes of 40 cases with concomitant exotropia who underwent strabismus correction at the Ophthalmology Department of Nantong University Hospital from October 2020 to July 2021 were included in this study, all of whom underwent unilateral lateral rectus recession combined with a medial rectus resection in the same eye. Aberration parameters were measured 1 day before surgery and 1 week, 1 month, 3 months, and 6 months after surgery. Differences in the indicators at each time period were compared by analysis of variance (ANOVA) of repeated measures data for a single factor, and data were analyzed using SPSS 25.0 statistical application software. Results: 5 mm pupil diameter: the preoperative and postoperative RMS of total aberration showed statistically significant difference (P < 0.01). Postoperation test (Bonferroni method) and preoperative comparison at each period after surgery showed statistically significant differences between 6 months after surgery (P=0.002) and preoperative comparison. The preoperative and postoperative comparison of RMS in LOAs was statistically significant (P < 0.01); postoperative test (Bonferroni method) and preoperative comparison showed that there were statistically significant differences between 1 week (P=0.033) and 6 months (P=0.002) after operation. The difference of RMS of defocus before and after operation was statistically significant (P < 0.01); postoperation test (Bonferroni method) and preoperative comparison showed that there was statistically significant difference between 6 months after operation (P=0.007) and preoperative comparison. There was statistically significant difference in preoperative and postoperative RMS of HOAs (P=0.013). Postoperative test (Bonferroni method) and preoperative comparison showed that there was statistically significant difference 6 months after surgery (P=0.03). The RMS of secondary astigmatism showed a statistically significant difference before and after operation (P=0.001), and the postoperation test (Bonferroni method) showed a statistically significant difference 6 months after operation (P=0.002). In 5 mm pupil diameter, the preoperative and postoperative RMS of total aberration showed statistically significant difference (P < 0.01), postoperative test (Bonferroni method) was used to compare each period after surgery with that before surgery, and there were statistically significant differences between 1 week after surgery (P=0.034), 3 months after surgery (P=0.033), and 6 months after surgery (P=0.003). The preoperative and postoperative comparison of RMS in LOAs was statistically significant (P < 0.01), postoperative test (Bonferroni method) was used to compare each period after surgery with that before surgery, and there were statistically significant differences between 1 week after surgery (P=0.04), 3 months after surgery (P=0.034), and 6 months after surgery (P=0.004). The difference of RMS of defocus before and after surgery was statistically significant (P=0.002), and the comparison between postoperation test (Bonferroni method) and preoperation showed that the difference was statistically significant 6 months after surgery (P=0.027). The RMS of astigmatism showed statistically significant difference before and after operation (P=0.002), and the postoperation test (Bonferroni method) showed statistically significant difference between 6 months after operation (P=0.009) and before operation. Conclusion: We found that horizontal rectus surgery had a transient effect on LOAs and almost no effect on HOAs. Long-term follow-up is recommended after strabismus surgery to observe eye position and binocular visual function. Because of the high prevalence of strabismus in adolescents, long-term observation of the eye axis and aberration is recommended.

Formononetin Improves the Survival of Random Skin Flaps Through PI3K/Akt-Mediated Nrf2 Antioxidant Defense System.

Random-pattern skin flap is widely used in plastic and reconstructive surgery. However, its clinical effect is limited by ischemia necrosis occurs at the distal part of flap. Previous studies have proved that the protective effect of formononetin was associated with its antioxidant, anti-inflammatory ability. However, further research is still needed on the effect of formononetin on flap viability. The purpose of our study was to investigate the effect of formononetin on flap survival and the underlying mechanisms. Two doses (25 mg/kg, 50 mg/kg)of formononetin were administered for seven consecutive days on flap model. Flap tissues were collected on postoperative day 7. Our results revealed that formononetin promoted skin flap viability in a dose-dependent manner. Using immunohistochemical staining and western blot, we found that formononetin significantly reduced oxidative stress and inflammation. Hematoxylin and eosin (H and E) staining, laser Doppler images and immunofluorescence staining showed the enhancement of angiogenesis after formononetin treatment. Mechanistically, we demonstrated that the antioxidation of formononetin was mediated by activation and nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2), while down-regulating cytoplasmic Kelch-like ECH-associated protein 1 (Keap1) expression. Co-treatment with formononetin and LY294002 (15 mg/kg), a potent Phosphatidylinositol-3-kinase (PI3K) inhibitor, which aborted nuclear Nrf2 expression and phosphorylated Akt, indicating that formononetin-mediated Nrf2 activation was related to PI3K/Akt pathway. Overall, our findings revealed that formononetin increased angiogenesis, reduced oxidative stress and inflammation, thus promoting flap survival. We highlighted the antioxidant effects of formononetin since the Nrf2 system was activated. Therefore, formononetin might be a promising candidate drug that can enhance survival of skin flaps.

Resveratrol Pretreatment Inhibits Myocardial Apoptosis in Rats Following Coronary Microembolization via Inducing the PI3K/Akt/GSK-3ß Signaling Cascade.

PURPOSE: Coronary microembolization (CME) is associated with progressive cardiac dysfunction, myocardial inflammation, and apoptosis. Resveratrol (RES) has a considerable role in cardioprotection. However, the contribution and possible mechanisms of RES in CME have not been clearly understood. METHODS: In the current study, 40 SD rats were randomly selected and categorized into various groups including CME, CME + resveratrol (CME + RES), CME + resveratrol+ LY294002 (CME + RES + LY), and sham groups (10 animals in each group). The inert plastic microspheres (42 µm) were injected into the rats' left ventricle for developing the CME model. Then resveratrol (25 mg/kg/d) was given to the rats in the CME + RES and CME + RES + LY groups for one week before CME induction. Furthermore, LY294002 (10 mg/kg) was intraperitoneally injected into the rats of the CME + RES + LY group 0.5 hours before CME modeling. The cardiac functions, serum levels of myocardial injury biomarkers, myocardial histopathology, and mRNA and proteins associated with myocardial apoptosis were all assessed 12 hours after surgery. RESULTS: The results revealed that resveratrol pretreatment alleviated the CME-induced myocardial damage by improving cardiac dysfunction, and lowering the serum level of myocardial injury biomarkers, myocardial microinfarct size, and cardiomyocyte apoptotic index. Pretreatment with resveratrol reduced the level of proteins and mRNAs associated with the pro-apoptosis in myocardial tissues and increased the levels of proteins and mRNAs associated with the anti-apoptosis. Moreover, the combined treatment of resveratrol and LY294002 reversed the observed protective effects. CONCLUSION: Resveratrol can inhibit cardiomyocyte apoptosis, thus attenuating the CME-induced myocardial injury by triggering the PI3K/Akt/GSK-3ß cascade.

miR-200a-3p Attenuates Coronary Microembolization-Induced Myocardial Injury in Rats by Inhibiting TXNIP/NLRP3-Mediated Cardiomyocyte Pyroptosis.

Coronary microembolization (CME) commonly develops as a complication after percutaneous coronary intervention (PCI), and associated inflammation is a leading driver of myocardial damage. Cardiomyocyte loss in the context of ischemic myocardial disease has been linked to inflammatory pyroptotic cell death. Additionally, miR-200a-3p dysregulation has been linked to myocardial ischemia-reperfusion and many other pathological conditions. However, how miR-200a-3p impacts cardiomyocyte pyroptosis in the context of CME remains to be assessed. Herein, a rat model of CME was established via the injection of microembolic spheres into the left ventricle. When myocardial tissue samples from these rats were analyzed, miR-200a-3p levels were markedly decreased, whereas thioredoxin-interacting protein (TXNIP) levels were increased. The ability of miR-200a-3p to directly target TXNIP and to control its expression was confirmed via dual-luciferase reporter assay. Adeno-associated virus serotype 9-pre-miR-200a-3p (AAV-miR-200a-3p) construct transfection was then employed as a means of upregulating this miRNA in CME model rats. Subsequent assays, including echocardiography, enzyme-linked immunosorbent assays (ELISAs), hematoxylin-eosin (H&E) staining, hematoxylin-basic fuchsin-picric acid (HBFP) staining, TdT-mediated dUTP nick-end labeling (TUNEL) staining, immunofluorescence staining, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blotting revealed that miR-200a-3p overexpression inhibited cardiomyocyte pyroptosis and alleviated CME-induced myocardial injury by inhibiting the TXNIP/NOD-like receptor family pyrin domain-containing 3 (NLRP3) pathway. The ability of miR-200a-3p to protect against CME-induced myocardial injury thus highlights a novel approach to preventing or treating such myocardial damage in clinical settings.

Breviscapine Pretreatment Inhibits Myocardial Inflammation and Apoptosis in Rats After Coronary Microembolization by Activating the PI3K/Akt/GSK-3ß Signaling Pathway.

PURPOSE: Coronary microembolization (CME) can cause myocardial inflammation, apoptosis and progressive cardiac dysfunction. On the other hand, breviscapine exerts a significant cardioprotective effect in many cardiac diseases although its role and the potential mechanisms in CME remain unclear. Therefore, the present study aimed to ascertain whether pretreatment with breviscapine could improve CME-induced myocardial injury by alleviating myocardial inflammation and apoptosis. The possible underlying mechanisms were also explored. METHODS: In this study, 48 Sprague-Dawley (SD) rats were randomly assigned to the CME, CME + breviscapine (CME + BE), CME + breviscapine + LY294002 (CME + BE + LY) and sham groups (12 rats per group). In addition, the CME model was successfully established by injecting 42 µm inert plastic microspheres into the left ventricle of rats. Rats in the CME + BE and CME + BE + LY groups received 40 mg/kg/d of breviscapine for 7 days before inducing CME. Moreover, rats in the CME + BE + LY group were intraperitoneally injected with the phosphoinositide 3-kinase (PI3K) specific inhibitor, LY294002 (10 mg/kg) 30 minutes before CME modeling. 12 h after surgery, the study measured cardiac function, the serum levels of markers of myocardial injury, myocardial inflammation-associated mRNAs and proteins, myocardial apoptosis-associated mRNAs and proteins and conducted myocardial histopathology. RESULTS: The findings demonstrated that pretreatment with breviscapine alleviated myocardial injury following CME by improving cardiac dysfunction, decreasing the serum levels of markers of myocardial injury, reducing the size of myocardial microinfarct and lowering the cardiomyocyte apoptotic index. More importantly, pretreatment with breviscapine resulted to a decrease in the levels of inflammatory and pro-apoptotic mRNAs and proteins in myocardial tissues and there was an increase in the levels of anti-apoptotic mRNAs and proteins. However, these protective effects were eliminated when breviscapine was combined with LY294002. CONCLUSION: The findings from this study indicated that breviscapine may inhibit myocardial inflammation and apoptosis by regulating the PI3K/protein kinase B (Akt)/glycogen synthase kinase-3ß (GSK-3ß) pathway, thereby ameliorating CME-induced cardiac dysfunction and reducing myocardial injury.

A new abietane mono-norditerpenoid from Podocarpus nagi.

A new abietane mono-norditerpenoid, nagiol A (1), along with three known diterpenoids were isolated from the leaves of Podocarpus nagi. Their structures were elucidated by means of extensive spectroscopic analysis. This is the first report of abietane mono-norditerpenoid separated from plant of the genus Podocarpus. Compound 1 was assessed for its cytotoxicity against five human tumour lines (HL-60, SMMC-7721, A-549, MCF-7 and SW-480), and the result showed that it had no activity.

A new naphthol from the twigs and leaves of Pterospermum yunnanense.

A new naphthol, 7-hydroxy-6-methyl-1-naphthoic acid methyl ester (1), together with eight known compounds, 6-hydroxy-7-(hydroxymethyl)-1-isopropyl-4-methyl-naphthalene (2), α-hydroxyacetosyringone (3), hexadecyl ferulate (4), scoparone (5), (+)-syringaresinol (6), stigmast-1,5-dien-3ß-ol (7), ß-sitosterol (8) and daucosterol (9), were isolated from the twigs and leaves of Pterospermum yunnanense Hsue. Their structures were elucidated by using spectroscopic analysis. All the compounds were isolated for the first time from P. yunnanense Hsue. Compound 1 was assessed for its cytotoxicity against five human tumour lines (HL-60, SMMC-7721, A-549, MCF-7 and SW-480), and the result showed that it has no activity.

Horsfiequinones A-F, dimeric diarylpropanoids from Horsfieldia tetratepala.

A new diarylpropanoid, horsfiequinone A (1), and five new dimeric diarylpropanoids with 1,4-p-benzoquinone residue, horsfiequinones B-F (2-6), along with a known compound, combrequinone B (7), were isolated from Horsfieldia tetratepala. Their structures were elucidated by means of spectroscopic analysis. Horsfiequinones B-F (2-6), isolated as enantiomer mixtures with unequal proportions, were verified by analysis on a chiral OD-H HPLC column. Cytotoxicity evaluation against five human tumor lines showed selective inhibitory effects on HL-60 for several compounds tested with IC50 values ranging from 3.18 ± 0.67 to 6.61 ± 0.08 µM.

trans-Diaqua-bis-[2-(2-pyrid-yl)acetato-κN,O]nickel(II).

In the centrosymmetric title complex, [Ni(C(7)H(6)NO(2))(2)(H(2)O)(2)], the Ni(II )atom, located on an inversion center, is six-coordinated in a distorted octa-hedral geometry defined by two N and four O atoms from the two chelating 2-(2-pyrid-yl)acetate ligands and two aqua ligands. The mol-ecules form a three-dimensional framework by O-H⋯O hydrogen bonds and aromatic π-π stacking inter-actions, with a centroid-centroid distance of 3.506 (3) Å.