Influence of bone wax on bone healing: a case report and literature review.

The purposes of this article are to report the clinical case of a patient who exhibited a foreign body reaction associated with the use of bone wax after extraction of an impacted third molar and to present an integrative literature review addressing the possible influences of this hemostatic agent on bone healing. A 26-year-old woman who underwent the extraction of her mandibular right third molar developed intense alveolar bleeding during surgery, requiring the use of bone wax. In the 2-month postoperative period, the patient presented with intraoral edema and discharge of a purulent secretion via the alveolar route. After cone beam computed tomographic images revealed increased hyperdensity inside the alveolus, alveolar curettage was performed and the material that was obtained was submitted to histopathologic examination. The results of the histopathologic analysis proved conclusive for an inflammatory foreign body reaction associated with exogenous material. A search of the PubMed, SciELO, and LILACS databases identified 22 studies that evaluated the influence of this hemostatic agent on bone healing, and an integrative review involving 367 animals and 75 humans was compiled. Bone wax is a nonresorbable material capable of negatively influencing bone healing. It is suggested that the product be used cautiously in amounts that are just enough to promote the sealing of the bone channels.

Glial cell derived neurotrophic factor prevents western diet and palmitate-induced hepatocyte oxidative damage and death through SIRT3.

Nonalcoholic fatty liver disease (NAFLD) is associated with increased oxidative stress that leads to hepatocyte and mitochondrial damage. In this study we investigated the mechanisms involved in the induction of oxidative stress and impairment of mitochondrial quality control and mitophagy in hepatocytes by the saturated fatty acid palmitate and Western diet feeding in mice and if their harmful effects could be reversed by the neurotrophic factor glial cell derived neurotrophic factor (GDNF). Western diet (WD)-feeding increased hepatic lipid peroxidation in control mice and, in vitro palmitate induced oxidative stress and impaired the mitophagic clearance of damaged mitochondria in hepatocytes. This was accompanied by reductions in hepatocyte sirtuin 3 (SIRT3) deacetylase activity, gene expression and protein levels as well as in superoxide dismutase enzyme activity. These reductions were reversed in the liver of Western diet fed GDNF transgenic mice and in hepatocytes exposed to palmitate in the presence of GDNF. We demonstrate an important role for Western diet and palmitate in inducing oxidative stress and impairing mitophagy in hepatocytes and an ability of GDNF to prevent this. These findings suggest that GDNF or its agonists may be a potential therapy for the prevention or treatment of NAFLD.

Low-grade elevation of palmitate and lipopolysaccharide synergistically induced ß-cell damage via inhibition of neutral ceramidase.

High concentrations of free fatty acids (FFAs) or lipopolysaccharide (LPS) could lead to ß-cell apoptosis and dysfunction, while low-grade elevation of FFAs or LPS, which are more common in people with type 2 diabetes mellitus (T2DM) or obesity, have no obvious toxic effect on ß-cells. Palmitate is a component closely related to metabolic disorders in FFAs. Recent studies have found that low-grade elevation of palmitate and LPS synergistically affects the sphingolipid signaling pathway by activating Toll-like receptor 4 (TLR4) and further enhances the expression of inflammatory cytokines in immune cells. Previous studies demonstrated that sphingolipids also played an important role in the occurrence and development of T2DM. This study aimed to investigate the synergistic effects of low-grade elevation of palmitate and LPS on viability, apoptosis and insulin secretion in the rat pancreatic ß-cell line INS-1 or islets and the role of sphingolipids in this process. We showed that low-grade elevation of palmitate or LPS alone did not affect the viability, apoptosis, glucose-stimulated insulin secretion (GSIS) or intracellular insulin content of INS-1 cells or islets, while the combination of the two synergistically inhibited cell viability, induced apoptosis and decreased basal insulin secretion in INS-1 cells or islets. Treatment with palmitate and LPS markedly upregulated TLR4 protein expression and downregulated neutral ceramidase (NCDase) activity and protein expression. Additionally, low-grade elevation of palmitate and LPS synergistically induced a significant increase in ceramide and a decrease in sphingosine-1-phosphate. Blocking TLR4 signaling or overexpressing NCDase remarkably attenuated INS-1 cell injury induced by the combination of palmitate and LPS. However, inhibition of ceramide synthase did not ameliorate injury induced by palmitate and LPS. Overall, we show for the first time that low-grade elevation of palmitate and LPS synergistically induced ß-cell damage by activating TLR4 signaling, inhibiting NCDase activity, and further modulating sphingolipid metabolism, which was different from a high concentration of palmitate-induced ß-cell injury by promoting ceramide synthesis.

Patchouli alcohol ameliorates skeletal muscle insulin resistance and NAFLD via AMPK/SIRT1-mediated suppression of inflammation.

Obesity-induced chronic low-grade inflammation and thus causes various metabolic diseases, such as insulin resistance and non-alcoholic fatty liver disease (NAFLD). Patchouli alcohol (PA), an active component extracted from patchouli, displayed anti-inflammatory effects on different cell types. However, the impact of PA on skeletal muscle insulin signaling and hepatic lipid metabolism remains unclear. This study aimed to investigate whether PA would affect insulin signaling impairment in myocytes and lipid metabolism in hepatocytes. Treatment with PA ameliorated palmitate-induced inflammation and aggravation of insulin signaling in C2C12 myocytes and lipid accumulation in HepG2 hepatocytes. Treatment of C2C12 myocytes and HepG2 cells with PA augmented AMP-activated protein kinase (AMPK) phosphorylation and Sirtuin 1 (SIRT1) expression in a dose-dependent manner. siRNA-mediated suppression of AMPK or SIRT1 mitigated the effects of PA on palmitate-induced inflammation and insulin resistance in C2C12 myocytes and lipid accumulation in HepG2 cells. Animal experiments demonstrated that PA administration increased AMPK phosphorylation and SIRT1 expression, and ameliorated inflammation, thereby attenuating skeletal muscle insulin resistance and hepatic steatosis in high-fat diet-fed mice. These results denote that PA alleviates skeletal muscle insulin resistance and hepatic steatosis through AMPK/SIRT1-dependent signaling. This study might provide a novel therapeutic approach for treating obesity-related insulin resistance and NAFLD.

Acetylcholine reduces palmitate-induced cardiomyocyte apoptosis by promoting lipid droplet lipolysis and perilipin 5-mediated lipid droplet-mitochondria interaction.

Lipid droplets (LDs), which are neutral lipid storage organelles, are important for lipid metabolism and energy homeostasis. LD lipolysis and interactions with mitochondria are tightly coupled to cellular metabolism and may be potential targets to buffer the effects of excessive toxic lipid species levels. Acetylcholine (ACh), the major neurotransmitter of the vagus nerve, exhibits cardioprotective effects. However, limited research has focused on its effects on LD lipolysis and the LD-mitochondria association in fatty acid (FA) overload models. Here, we reveal that palmitate (PA) induces an increase in expression of the FA transport protein cluster of differentiation 36 (CD36) and LD formation; remarkably reduces the expression of lipases involved in triacylglycerol (TAG) lipolysis, such as adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL) and monoacylglycerol lipase (MGL); impairs LD-mitochondria interaction; and decreases perilipin 5 (PLIN5) expression, resulting in LD accumulation and mitochondrial dysfunction, which ultimately lead to cardiomyocyte apoptosis. ACh significantly upregulates PLIN5 expression and improved LD lipolysis and the LD-mitochondria association. Moreover, ACh reduces CD36 expression, LD deposition and mitochondrial dysfunction, ultimately suppressing apoptosis in PA-treated neonatal rat ventricular cardiomyocytes (NRVCs). Knockdown of PLIN5, which plays a role in LD-mitochondria contact site formation, abolishes the protective effects of ACh in PA-treated NRVCs. Thus, ACh protects cardiomyocytes from PA-induced apoptosis, at least partly, by promoting LD lipolysis and activating LD-mitochondria interactions via PLIN5. These findings may aid in developing novel therapeutic approaches that target LD lipolysis and PLIN5-mediated LD-mitochondria interactions to prevent or alleviate lipotoxic cardiomyopathy.

Capmatinib improves insulin sensitivity and inflammation in palmitate-treated C2C12 myocytes through the PPARδ/p38-dependent pathway.

Capmatinib (CAP) has been used to treat metastatic non-small lung cancer (NSCL) and suppress inflammation. It causes hypoglycemia in NSCL patients. Therefore, it is expected that CAP improves inflammation-mediated insulin resistance due to its anti-inflammatory effect. However, the impacts of CAP on insulin signaling in skeletal muscle cells have not yet been fully elucidated. Herein, we investigated the effect of CAP on insulin resistance in palmitate-treated C2C12 myocytes and explored the related molecular mechanisms. We found that treatment of C2C12 myocytes with CAP reversed palmitate-induced impairment of insulin signaling and glucose uptake. CAP treatment ameliorated phosphorylation of inflammatory markers, including NFκB and IκB, in palmitate-treated C2C12 myocytes. Further, it augmented PPARδ expression and suppressed palmitate-induced p38 phosphorylation in a dose-dependent manner. siRNA-mediated suppression of PPARδ abolished the effects of CAP on palmitate-induced insulin resistance and inflammation as well as p38 phosphorylation. Therefore, it has been shown that CAP treatment ameliorates insulin resistance in palmitate-treated C2C12 myocytes via PPARδ/p38 signaling-mediated suppression of inflammation. These results may represent a novel therapeutic approach that could halt insulin resistance and type 2 diabetes.

The Ca2+ -binding protein sorcin stimulates transcriptional activity of the unfolded protein response mediator ATF6.

Sorcin is a calcium-binding protein involved in maintaining endoplasmic reticulum (ER) Ca2+ stores. We have previously shown that overexpressing sorcin under the rat insulin promoter was protective against high-fat diet-induced pancreatic beta-cell dysfunction in vivo. Activating transcription factor 6 (ATF6) is a key mediator of the unfolded protein response (UPR) that provides cellular protection during the progression of ER stress. Here, using nonexcitable HEK293 cells, we show that sorcin overexpression increased ATF6 signalling, whereas sorcin knock out caused a reduction in ATF6 transcriptional activity and increased ER stress. Altogether, our data suggest that sorcin downregulation during lipotoxic stress may prevent full ATF6 activation and a normal UPR during the progression of obesity and insulin resistance.

Blocking TLR4-NF-κB pathway protects mouse islets from the combinatorial impact of high fat and fetuin-A mediated dysfunction and restores ability for insulin secretion.

Lipid mediated pancreatic ß-cell dysfunction during Type 2 diabetes is known to be regulated by activation of TLR4 (Toll Like Receptor 4) and NF-κB (Nuclear factor kappa B). Recently we have reported that MIN6 cells (mouse insulinoma cells) secrete fetuin-A on stimulation by palmitate that aggravates ß-cell dysfunction, but the mechanism involved in-vivo has not been demonstrated and thus remained unclear. Here we attempted to dissect the role of palmitate and fetuin-A on insulin secretion using high fat diet (HFD) fed mice model. HFD islets showed curtailed insulin secretion after 20 weeks of treatment with activated TLR4-NF-κB pathway. Further treatment of islets with palmitate raised fetuin-A expression by ~2.8 folds and cut down insulin secretion by ~1.4 folds. However, blocking the activity of TLR4, fetuin-A and NF-κB using specific inhibitors or siRNAs not only restored insulin secretion by ~2 folds in standard diet fed mice islets and MIN6 cells but also evoke insulin secretory ability by ~2.3 folds in HFD islets. Altogether this study demonstrated that blocking TLR4, fetuin-A and NF-κB protect pancreatic ß-cells from the negative effects of free fatty acid and fetuin-A and restore insulin secretion.

Unusual complications of bone wax at the skull base.

OBJECTIVE: This study aimed to describe the clinical presentation, microbiological profile and management of complications of bone wax usage for surgical procedures at the skull base. METHOD: The case records of a series of five patients who developed post-operative surgical site complications because of bone wax usage during skull base surgery were reviewed. RESULTS: In all five patients, persistent site-specific clinical features were noted along with intra-operative presence of excessive bone wax. Three unique cases of presentation, one with a fungal brain abscess because of Aspergillus flavus infection, another with fungal osteomyelitis because of Trichosporon beigelii infection and a third with intradural migration of bone wax into the cerebellopontine angle cistern are highlighted. CONCLUSION: The presentation of surgical site infection at the skull base because of excessive use of bone wax can be manifold. The need for testing appropriate cultures including fungal culture is highlighted.

Dietary saturated fatty acid palmitate promotes cartilage lesions and activates the unfolded protein response pathway in mouse knee joints.

Increased intake of dietary saturated fatty acids has been linked to obesity and the development of Osteoarthritis (OA). However, the mechanism by which these fats promote cartilage degradation and the development of OA is not clearly understood. Here, we report the effects of consumption of common dietary saturated and unsaturated fatty acids, palmitate and oleate, respectively, on body weight, metabolic factors, and knee articular cartilage in a mouse model of diet-induced obesity. Mice fed on a diet rich in saturated or unsaturated fatty acid gained an equal amount of weight; however, mice fed a palmitate diet, but not a control or oleate diet, exhibited more cartilage lesions and increased expression of 1) unfolded protein response (UPR)/endoplasmic reticulum (ER) stress markers including BIP, P-IRE1α, XBP1, ATF4, and CHOP; 2) apoptosis markers CC3 and C-PARP; and 3) negative cell survival regulators Nupr1 and TRB3, in knee articular cartilage. Palmitate-induced apoptosis was confirmed by TUNEL staining. Likewise, dietary palmitate was also increased the circulatory levels of classic proinflammatory cytokines, including IL-6 and TNF-α. Taken together, our results demonstrate that increased weight gain is not sufficient for the development of obesity-linked OA and suggest that dietary palmitate promotes UPR/ER stress and cartilage lesions in mouse knee joints. This study validates our previous in vitro findings and suggests that ER stress could be the critical metabolic factor contributing to the development of diet/obesity induced OA.

Trimetazidine improves hepatic lipogenesis and steatosis in non­alcoholic fatty liver disease via AMPK­ChREBP pathway.

Clinical studies have demonstrated that trimetazidine (TMZ) possesses a synergistic hypolipidemic effect together with statins, but the underlying mechanism remains to be elucidated. The present study aimed to investigate the role of TMZ in non­alcoholic fatty liver disease (NAFLD). By investigating the TMZ treatment of NAFLD, it was identified that high­fat diet (HFD) mice exhibit significant changes in several physiologic indices, including body weight, plasma lipids and glucose tolerance. Notably, hepatocyte bullous steatosis and fibrosis in HFD mice are greatly attenuated by 8 weeks of TMZ treatments. The results of the present study also indicated that the expression of carbohydrate­responsive element­binding protein (ChREBP), fatty acid synthase and acetyl­CoA carboxylase were all significantly reduced in the HFD + TMZ group compared with the HFD group. In order to confirm the hypothesis in vitro, the palmitate­treated liver cancer cell line (HepG2) was employed and similar results were obtained in TMZ­treated HepG2 cells. Furthermore, TMZ markedly upregulated the AMP­activated protein kinase (AMPK) signaling pathway and reduced the expression of forkhead box O1 (FOXO1) in the cells, while these effects controlled by TMZ were abolished by the AMPK inhibitor Compound C. The present study reported that knockdown of FOXO1 expression by FOXO1 small interfering RNA resulted in a reduction of ChREBP protein expression and post­transcriptional activity. In summary, for the first time, to the best of the authors' knowledge, the present study revealed a novel role of TMZ in hepatic steatosis; TMZ ameliorated ChREBP­induced de novo lipogenesis by activating the AMPK­FOXO1 pathway.

Rg1 protects H9C2 cells from high glucose-/palmitate-induced injury via activation of AKT/GSK-3ß/Nrf2 pathway.

Our previous studies have assessed ginsenoside Rg1 (Rg1)-mediated protection in a type 1 diabetes rat model. To uncover the mechanism through which Rg1 protects against cardiac injury induced by diabetes, we mimicked diabetic conditions by culturing H9C2 cells in high glucose/palmitate. Rg1 had no toxic effect, and it alleviated the high glucose/palmitate damage in a dose-dependent manner, as indicated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and lactate dehydrogenase release to the culture medium. Rg1 prevented high glucose/palmitate-induced cell apoptosis, assessed using cleaved caspase-3 and terminal deoxynucleotidyl transferase dUTP nick end labelling staining. Rg1 also reduced high glucose-/palmitate-induced reactive oxygen species formation and increased intracellular antioxidant enzyme activity. We found that Rg1 activates protein kinase B (AKT)/glycogen synthase kinase-3 (GSK-3ß) pathway and antioxidant nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, indicated by increased phosphorylation of AKT and GSK-3ß, and nuclear translocation of Nrf2. We used phosphatidylinositol-3-kinase inhibitor Ly294002 to block the activation of the AKT/GSK-3ß pathway and found that it partially reversed the protection by Rg1 and decreased Nrf2 pathway activation. The results suggest that Rg1 exerts a protective effect against high glucose and palmitate damage that is partially AKT/GSK-3ß/Nrf2-mediated. Further studies are required to validate these findings using primary cardiomyocytes and animal models of diabetes.

Effect of cis- and trans-Monounsaturated Fatty Acids on Palmitate Toxicity and on Palmitate-induced Accumulation of Ceramides and Diglycerides.

Dietary trans fatty acids (TFAs) have been implicated in serious health risks, yet little is known about their cellular effects and metabolism. We aim to undertake an in vitro comparison of two representative TFAs (elaidate and vaccenate) to the best-characterized endogenous cis-unsaturated FA (oleate). The present study addresses the possible protective action of TFAs on palmitate-treated RINm5F insulinoma cells with special regards to apoptosis, endoplasmic reticulum stress and the underlying ceramide and diglyceride (DG) accumulation. Both TFAs significantly improved cell viability and reduced apoptosis in palmitate-treated cells. They mildly attenuated palmitate-induced XBP-1 mRNA cleavage and phosphorylation of eukaryotic initiation factor 2α (eIF2α) and stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK), but they were markedly less potent than oleate. Accordingly, all the three unsaturated FAs markedly reduced cellular palmitate incorporation and prevented harmful ceramide and DG accumulation. However, more elaidate or vaccenate than oleate was inserted into ceramides and DGs. Our results revealed a protective effect of TFAs in short-term palmitate toxicity, yet they also provide important in vitro evidence and even a potential mechanism for unfavorable long-term health effects of TFAs compared to oleate.

Fucoxanthin alleviates palmitate-induced inflammation in RAW 264.7 cells through improving lipid metabolism and attenuating mitochondrial dysfunction.

In this study, we aimed to examine the effects of fucoxanthin on inflammation triggered by palmitate in macrophages. Raw 264.7 cells were treated with palmitate with or without fucoxanthin co-treatment. Fucoxanthin greatly alleviated palmitate-induced decrease in cell viability and loss of mitochondrial membrane potential. Fucoxanthin also significantly attenuated the palmitate-induced transcriptional expression of Il-6, Il-1ß, Tnfα and Nlrp3 inflammasomes and increased the expression of Tgfb. In addition, fucoxanthin decreased triglyceride accumulation induced by palmitate through enhancing the expression of Cpt1a, Pparg and other lipid metabolism genes. Inhibition of CPT1a by etomoxir attenuated the anti-inflammatory effect of fucoxanthin. Furthermore, fucoxanthin increased AMPK phosphorylation and AMPKa1 knockdown by its specific siRNA diminished protective function. In addition, fucoxanthin restored palmitate-mediated mitochondrial dysfunction and improved mitophagy-related gene expression. These findings suggest that fucoxanthin could attenuate free fatty acid-induced inflammation in macrophages through modulating lipid metabolism and mitigating mitochondrial dysfunction.

Hepatocyte-specific Nrf2 deficiency mitigates high-fat diet-induced hepatic steatosis: Involvement of reduced PPARγ expression.

Non-alcoholic fatty liver disease (NAFLD) is an emerging global disease with increasing prevalence. However, the mechanism of NAFLD development is not fully understood. To elucidate the cell-specific role of nuclear factor erythroid-derived 2-like 2 (NRF2) in the pathogenesis of NAFLD, we utilized hepatocyte- and macrophage-specific Nrf2-knockout [Nrf2(L)-KO and Nrf2(Mϕ)-KO] mice to examine the progress of NAFLD induced by high-fat diet (HFD). Compared to Nrf2-LoxP littermates, Nrf2(L)-KO mice showed less liver enlargement, milder inflammation and less hepatic steatosis after HFD feeding. In contrast, Nrf2(Mϕ)-KO mice displayed no significant difference in HFD-induced hepatic steatosis from Nrf2-LoxP control mice. Mechanistic investigations revealed that Nrf2 deficiency in hepatocytes dampens the expression of peroxisome proliferator-activated receptor γ (PPARγ) and its downstream lipogenic genes in the liver and/or primary hepatocytes induced by HFD and palmitate exposure, respectively. While PPARγ agonists augmented PPARγ expression and its transcriptional activity in primary hepatocytes in a NRF2-dependent manner, forced overexpression of PPARγ1 or γ2 distinctively reversed the decreased expression of their downstream genes fatty acid binding protein 4, lipoprotein lipase and/or fatty acid synthase caused by Nrf2 deficiency. We conclude that NRF2-dependent expression of PPARγ in hepatocytes is a critical initiating process in the development of NAFLD, suggesting that inhibition of NRF2 specifically in hepatocytes may be a valuable approach to prevent the disease.

Chronic inflammatory reaction to bone wax in cochlear implantation: A case report and literature review.

Background: Cochlear implantation is a well-established treatment for severe-to-profound sensorineural hearing loss. While bone wax is used commonly during mastoidectomy and other bony surgeries as a hemostatic agent, there have been reports of bone wax triggering foreign body reactions, months to years after surgery. This report describes the first known foreign body reaction to bone wax used in cochlear implantation surgery. Case Presentation: A 6-year-old male presented with an unusual post-auricular inflammation two years after cochlear implantation. Extended treatment with oral and intravenous antibiotics failed to resolve the presumed infection. Upon exploration of the mastoid cavity, fragments of bone wax were discovered within the granulation tissue. Excision of bone wax fragments and local flap reconstruction resulted in complete resolution of the inflammatory process. Conclusions: Bone wax has been implicated in foreign body reactions in many different surgical specialties. This is the first reported case of an adverse reaction to bone wax after cochlear implantation. Clinically, the bone wax reaction was misinterpreted as an implant infection, which resulted in extended antibiotic use and delay of appropriate treatment. As a result, bone wax should be used judiciously during mastoidectomy, and particularly in the area of the electrode and soft tissue closure.

Chronic, Symptomatic Orbital Inflammation Resulting From Retained Bone Wax.

A 58-year-old man presented with a 9-month history of a chronically draining surgical wound and low-grade periorbital inflammation following a right lateral orbitotomy. Imaging of the right orbit revealed a peculiar lesion in the right lateral orbit that was hypointense on both T1- and T2-weighted MRI with peripheral enhancement. Exploratory orbitotomy and biopsy established the diagnosis of a chronic foreign body inflammatory reaction to bone wax; symptoms resolved following evacuation of the retained foreign material.A 58-year-old man developed a chronic, symptomatic, inflammatory reaction to bone wax following a lateral orbitotomy; only once previously has symptomatic orbital inflammation following orbital surgery as a result of bone wax been reported.

Taurine-Rich-Containing Hot Water Extract of Loliolus Beka Gray Meat Scavenges Palmitate-Induced Free Radicals and Protects Against DNA Damage in Insulin Secreting ß-Cells.

The loss of pancreatic ß-cells plays a central role in the pathogenesis of both type 1 and type 2 diabetes, and many studies have been focused on ways to improve glucose homeostasis by preserving, expanding and improving the function of ß-cell. Elevated levels of free fatty acids such as palmitate might contribute to the loss of ß-cells. A marine squid, Loliolus beka has long been used as a food in Korea, China, Japan and Europe due to its tender meat and high taurine content. Here, we investigated the protective effects of a hot water extract of Loliolus beka meat (LBM) against palmitate toxicity in Ins-1 cells, a rat ß-cell line. Treatment with LBM extract protected against palmitate-induced cytotoxicity and scavenged overproduction of nitric oxide, alkyl, and hydroxyl radicals. In addition, LBM extract protected against palmitate-induced DNA damage and ß-cell dysfunction. These findings suggest that LBM protects pancreatic ß-cells from palmitate-induced damage. LBM could be a potential therapeutic functional food for diabetes.

Curcumin­loaded PEG­PDLLA nanoparticles for attenuating palmitate­induced oxidative stress and cardiomyocyte apoptosis through AMPK pathway.

Curcumin (CUR) has the ability to attenuate oxidative stress in the myocardium and to protect the myocardium from lipotoxic injury owing to its lipid­reducing properties. However, the use of CUR is limited due to its hydrophobicity and instability. In this study, CUR­loaded nanoparticles (CUR NPs) were developed using an amphiphilic copolymer, monomethoxy poly (ethylene glycol)­b­poly (DL­lactide), as a vehicle material. CUR NPs with high drug loading and small size were prepared under optimized conditions. The effects of CUR NPs on palmitate­induced cardiomyocyte injury were investigated and the possible protective mechanism of CUR NPs was also examined. It was found that CUR NPs were able to control the release of CUR and to deliver CUR to H9C2 cells, and they could prevent palmitate­treated H9C2 cells from apoptosis. In addition, CUR NPs could regulate the Bax and Bcl­2 levels of palmitate­treated H9C2 cells back to their respective normal levels. A prospective mechanism for the function of CUR NPs is that they may activate the AMP­activated protein kinase (AMPK)/mammalian target of rapamycin complex­1/p­p70 ribosomal protein S6 kinase signaling pathway, regulate the expression of downstream proteins and resist the palmitate­induced cardiomyocyte injury. Results suggest that CUR NPs can attenuate palmitate­induced oxidative stress in cardiomyocytes and protect cardiomyocytes from apoptosis through the AMPK pathway. In view of the safety and efficiency of these CUR NPs, they have potential for application in protecting the myocardium from lipotoxic injury.