Myocardial Ischemia Recruits Mechanically Insensitive Cardiac Sympathetic Afferents in Cats

2002 ◽  
Vol 87 (2) ◽  
pp. 660-668 ◽  
Author(s):  
Hui-Lin Pan ◽  
Shao-Rui Chen
Keyword(s):  
Lactic Acid ◽  
Myocardial Ischemia ◽  
Receptive Field ◽  
Topical Application ◽  
Dependent Manner ◽  
Mechanical Stimuli ◽  
Concentration Dependent Manner ◽  
C Fibers ◽  
Cardiac Afferents ◽  
New Evidence

Chest pain caused by myocardial ischemia is mediated by cardiac sympathetic afferents. Although silent nociceptors exist in somatic structures and some visceral organs, their presence in the heart remains uncertain. The present study examined the presence and the functional characteristics of mechanically insensitive cardiac sympathetic afferents using an electrical search technique. Single-unit activity of afferents innervating the left ventricle was recorded from the sympathetic chain in anesthetized cats. Cardiac afferents were identified initially with a stimulating electrode placed on the surface of the heart. Responses of cardiac afferents to mechanical stimuli, 5 min of myocardial ischemia, and topical application of bradykinin (1–10 μg/ml) and lactic acid (10–50 μg/ml) were then determined. Ischemia activated all 38 mechanically insensitive afferents and 17 of 25 mechanically sensitive afferents. The mechanically sensitive afferents typically were spontaneously active and had a smaller receptive field and a slightly faster conduction velocity. On the other hand, the mechanically insensitive afferents were slow conducting C fibers and had a large electrical receptive field on the epicardium. The response of 38 mechanically insensitive afferents to ischemia [2.83 ± 0.14 (SD) imp/s] was significantly greater than that of 17 mechanically sensitive afferents (from 0.41 ± 0.05 to 0.74 ± 0.15 imp/s). The mechanically insensitive afferents also exhibited a greater response to topical application of bradykinin or lactic acid in a concentration-dependent manner. This study provides important new evidence that the heart is innervated by silent sympathetic afferents, which are activated profoundly by myocardial ischemia. These data also suggest that the mechanically insensitive sympathetic afferents may function as cardiac nociceptors.

scholarly journals A new function for ATP: activating cardiac sympathetic afferents during myocardial ischemia

2010 ◽  
Vol 299 (6) ◽  
pp. H1762-H1771 ◽  
Author(s):  
Liang-Wu Fu ◽  
John C. Longhurst
Keyword(s):  
Myocardial Ischemia ◽  
Cardiovascular Responses ◽  
P2 Receptors ◽  
Nerve Fibers ◽  
Disulfonic Acid ◽  
Dependent Manner ◽  
P2 Receptor ◽  
C Fibers ◽  
Spinal Afferents ◽  
Cardiac Afferents

Myocardial ischemia activates cardiac sympathetic afferents leading to chest pain and reflex cardiovascular responses. Brief myocardial ischemia leads to ATP release in the interstitial space. Furthermore, exogenous ATP and α,β-methylene ATP (α,β-meATP), a P2X receptor agonist, stimulate cutaneous group III and IV sensory nerve fibers. The present study tested the hypothesis that endogenous ATP excites cardiac afferents during ischemia through activation of P2 receptors. Nerve activity of single unit cardiac sympathetic afferents was recorded from the left sympathetic chain or rami communicates (T2-T5) in anesthetized cats. Single fields of 45 afferents (conduction velocities = 0.25–4.92 m/s) were identified in the left ventricle with a stimulating electrode. Five minutes of myocardial ischemia stimulated 39 of 45 cardiac afferents (8 Aδ, 37 C fibers). Epicardial application of ATP (1–4 μmol) stimulated six ischemically sensitive cardiac afferents in a dose-dependent manner. Additionally, epicardial ATP (2 μmol), ADP (2 μmol), a P2Y agonist, and α,β-meATP (0.5 μmol) significantly activated eight other ischemically sensitive afferents. Third, pyridoxal phosphate-6-azophenyl-2′,4′-disulfonic acid, a P2 receptor antagonist, abolished the responses of six afferents to epicardial ATP (2 μmol) and attenuated the ischemia-related increase in activity of seven other afferents by 37%. In the absence of P2 receptor blockade, cardiac afferents responded consistently to repeated application of ATP ( n = 6) and to recurrent myocardial ischemia ( n = 6). Finally, six ischemia-insensitive cardiac spinal afferents did not respond to epicardial ATP (2–4 μmol), although these afferents did respond to epicardial bradykinin. Taken together, these data indicate that, during ischemia, endogenously released ATP activates ischemia-sensitive, but not ischemia-insensitive, cardiac spinal afferents through stimulation of P2 receptors likely located on the cardiac sensory neurites.

Acute Effect of an Incision on Mechanosensitive Afferents in the Plantar Rat Hindpaw

2002 ◽  
Vol 87 (2) ◽  
pp. 712-720 ◽  
Author(s):  
Minna M. Hämäläinen ◽  
G. F. Gebhart ◽  
Timothy J. Brennan
Keyword(s):  
Receptive Field ◽  
Background Activity ◽  
Response Magnitude ◽  
Field Size ◽  
Response Threshold ◽  
Mechanical Stimuli ◽  
Receptive Field Size ◽  
C Fibers ◽  
Afferent Fibers ◽  
Aβ Fibers

The purpose of this study was to examine which primary afferent fibers are sensitized to mechanical stimuli after an experimental surgical incision to the glabrous skin of the rat hindpaw. Afferent fibers teased from the L5dorsal root or the tibial nerve were recorded in anesthetized rats. The mechanical response properties of each fiber were characterized before and 45 min after an incision (or sham procedure) within the mechanical receptive field. Sensitization is characterized by an expansion of the mechanical receptive field, an increase in background activity, an increase in response magnitude, or a decrease in response threshold. After incision, the background activity and response properties of Aβ-fibers ( n = 9) to mechanical stimuli were unchanged. Four of 13 mechanosensitive Aδ-fibers exhibited sensitization after the incision; response threshold decreased, response magnitude increased, or receptive field size increased. Background activity of Aδ-fibers was not increased by the incision. Sensitization was observed in 4 of 18 mechanosensitive C-fibers 45 min after the incision. Background activity of C-fibers was not increased by the incision. In a group of mechanically insensitive afferent fibers (MIAs), 3 of 7 Aδ-fibers and 4 of 10 C-fibers sensitized 45 min after incision. Response threshold was decreased in only 2 of 17 MIAs; receptive field size increased in 7 of 17 MIAs. Aβ-fibers did not sensitize after the incision, and only 8 of 31 (26%) mechanosensitive Aδ- and C-fibers gave evidence of sensitization. In a group of MIA Aδ- and C-fibers, a greater percentage of 17 fibers studied (41%) were sensitized after incision. In this model, the principal effect of an incision, when examined 45 min after the insult, is an increase in receptive field size of the afferents, particularly those characterized as MIAs. To the extent that the mechanical hyperalgesia characterized in the same model is initiated in the periphery, it would appear that spatial summation of modestly increased response magnitude is important to the development of hyperalgesia.

Histamine Contributes to Ischemia-Related Activation of Cardiac Spinal Afferents: Role of H1 Receptors and PKC

2005 ◽  
Vol 93 (2) ◽  
pp. 713-722 ◽  
Author(s):  
Liang-Wu Fu ◽  
Walter Schunack ◽  
John C. Longhurst
Keyword(s):  
Myocardial Ischemia ◽  
Receptor Agonist ◽  
Visceral Afferents ◽  
Cardiovascular Reflexes ◽  
Dependent Manner ◽  
Endogenous Histamine ◽  
Nociceptive Information ◽  
Spinal Afferents ◽  
Cardiac Afferents

Myocardial ischemia activates cardiac spinal afferents that transmit the nociceptive information leading to chest pain and elicit excitatory cardiovascular reflexes. Previous studies have shown that histamine is increased in coronary sinus blood during myocardial ischemia and that this autacoid stimulates abdominal visceral afferents. The present investigation evaluated the role of endogenous histamine in stimulation of ischemically sensitive cardiac spinal afferents. Nerve activity of single-unit cardiac afferents was recorded from the left sympathetic chain or rami communicans (T2–T5) in anesthetized cats. Sixty-four cardiac afferents were identified. Injection (5–30 μg/kg) of histamine into the left atrium (LA) stimulated 7 ischemically sensitive cardiac afferents resulting in a significant increase in their activity in a dose-dependent manner. Also, LA injection of histamine (10 μg/kg) stimulated 7 of 8 ischemically insensitive cardiac spinal afferents. Administrations of 2-(3-chlorophenyl)histamine (250 μg/kg, LA), a specific H1 receptor agonist and histamine (10 μg/kg, LA), stimulated 9 other ischemically sensitive cardiac afferents (0.48 ± 0.10 to 1.40 ± 0.20 imp/s). In contrast, dimaprit (500 μg/kg, LA), an H2 receptor agonist, stimulated only one of the 9 afferents and thus did not alter their overall activity (0.40 ± 0.09 to 0.54 ± 0.09 imp/s). ( R)α-Methyl-histamine (500 μg/kg, LA), an H3 receptor agonist, did not stimulate any of the 9 afferents. Pyrilamine (300 μg/kg, iv), a selective H1 receptor antagonist, attenuated the activity of 8 afferents during 5 min of ischemia from 3.32 ± 0.38 to 1.87 ± 0.28 imp/s and abolished the response of 9 other cardiac afferents to histamine. Finally, administration of PKC-(19–36) (30 μg/kg, iv), a selective inhibitor of protein kinase C, attenuated the response of 8 cardiac afferents to histamine by 32%. These data indicate that endogenous histamine contributes to activation of cardiac sympathetic afferents during myocardial ischemia through H1 receptors and that the action of histamine on these cardiac afferents is partially dependent on the intracellular PKC pathway.

Direct Effects of Ropivacaine and Bupivacaine on Spinal Pial Vessels in Canine 

1997 ◽  
Vol 87 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Hiroki Iida ◽  
Yukinaga Watanabe ◽  
Shuji Dohi ◽  
Tadahiko Ishiyama
Keyword(s):  
Topical Application ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Beta Adrenoceptor ◽  
Pial Vessels ◽  
Arterial Blood ◽  
Before And After ◽  
Pial Arterioles ◽  
Anesthetized Dogs ◽  
Pial Vessel

Background Ropivacaine produces a vasoconstriction of cutaneous vessels in contrast to vasodilation produced by bupivacaine. To evaluate direct spinal microvascular actions of these local anesthetics, the authors investigated the concentration-related effects of ropivacaine and bupivacaine on spinal pial vascular diameters using the spinal window technique. Methods Anesthetized dogs (n = 14) divided into two groups (ropivacaine, n = 7; bupivacaine, n = 7) were prepared for measurement of spinal pial vessel diameters by intravital microscopy in a spinal window preparation. The authors administered six concentrations of each drug (10(-8)-10(-3) M) under the window and directly measured the spinal pial arteriolar and venular diameters at sequential times. Physiologic data including mean arterial blood pressure (MAP) and heart rate (HR) were determined before and after topical application of each concentration of the drugs. In additional experiments (n = 18), the action of topical ropivacaine and bupivacaine solution on spinal vessels was evaluated in the presence of yohimbine, prazosin, and propranolol. Results Ropivacaine significantly constricted whereas bupivacaine dilated pial arterioles and venules, both in a concentration-dependent manner. Microvascular alteration was not blocked with any of the adrenoceptor antagonists tested (yohimbine, prazosin, propranolol), each of which per se did not affect pial vessel diameters. Topical application of ropivacaine or bupivacaine did not induce any change in MAP or HR. Conclusions The present results indicate that ropivacaine constricts and bupivacaine dilates the pial vessels of the spinal cord in a concentration-dependent fashion, and the mechanisms involved in such actions do not seem to be mediated via alpha- or beta-adrenoceptor of spinal vasculature.

scholarly journals Development of Antibacterial Biocomposites Based on Poly(lactic acid) with Spice Essential Oil (Pimpinella anisum) for Food Applications

Polymers ◽  
2021 ◽  
Vol 13 (21) ◽  
pp. 3791
Author(s):  
Negin Noori ◽  
Ali Khanjari ◽  
Mohammadreza Rezaeigolestani ◽  
Ioannis K. Karabagias ◽  
Sahar Mokhtari
Keyword(s):  
Lactic Acid ◽  
Essential Oil ◽  
Food Packaging ◽  
Water Vapor Permeability ◽  
Principal Component ◽  
Poly Lactic Acid ◽  
Vapor Permeability ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Active Food Packaging

Among the main biodegradable food packaging materials, poly-lactic acid (PLA) is a commercially successful polymer used notably in the food packaging industry. In this study, active PLA films containing different percentage of anise essential oil (AE) (0, 0.5, 1 and 1.5% v/v) were developed, and characterized by physical, mechanical and antibacterial analysis. Based on physical examinations, thermal stability of PLA/AE films was greater than the neat PLA film, and the minimum water vapor permeability (WVP) was recorded for PLA/0.5AE film (1.29 × 10 11 g/m s), while maximum WVP was observed for PLA/1.5AE (2.09 × 1011 g/m s). Moreover, the lightness and yellowness of the composites were decreased by the addition of AE. For the PLA composites with 1.5% AE, the tensile strength decreased by 35% and the elongation break increased by 28.09%, comparing to the pure PLA. According to the antibacterial analysis, the minimum inhibitory concentrations of PLA/AE film were 5 to 100 mg/mL and the active composite could create visible inhibition zones of 14.2 to 19.2 mm. Furthermore, the films containing AE inhibited L. monocytogenes and V. parahaemolyticus in a concentration-dependent manner. The confirmation of the success of the incorporation of EOs into the PLA films was further evaluated using principal component analysis, where positive results were obtained. In this context, our findings suggest the significant potency of AE to be used as an antibacterial agent in active food packaging.

scholarly journals Bradykinin and thromboxane A2 reciprocally interact to synergistically stimulate cardiac spinal afferents during myocardial ischemia

2010 ◽  
Vol 298 (1) ◽  
pp. H235-H244 ◽  
Author(s):  
Liang-Wu Fu ◽  
John C. Longhurst
Keyword(s):  
Myocardial Ischemia ◽  
Nerve Activity ◽  
C Fibers ◽  
First Response ◽  
Complex Process ◽  
Rami Communicantes ◽  
The Individual ◽  
Spinal Afferents ◽  
Cardiac Afferents ◽  
Afferent Response

Myocardial ischemia is a complex process leading to the simultaneous release of a number of mediators, including thromboxane A2 (TxA2) and bradykinin (BK), that activate cardiac spinal afferents. The present study tested the hypothesis that TxA2 and BK reciprocally interact to excite ischemically sensitive cardiac afferents. Nerve activity of single cardiac afferent units was recorded from the left sympathetic chain or rami communicantes (T2–T5) of anesthetized cats. Fifty-two ischemically sensitive afferents (conduction velocity = 0.27–3.35 m/s, 7 Aδ-fibers and 45 C-fibers) were identified. Repeated injections (1 μg) of BK into the left atrium (LA) 4 min after the administration of U-46619 (5 μg into the LA), a TxA2 mimetic, induced a significantly larger cardiac afferent response than the first response to BK (0.61 ± 0.14 to 1.95 ± 0.29 vs. 0.66 ± 0.09 to 2.75 ± 0.34 impulses/s, first injection vs. second injection, n = 8). Conversely, blockade of TxA2 receptors with BM-13,177 (30 mg/kg iv) attenuated the responses of eight other afferents to BK (1 μg into the LA) by 45%. In contrast, repeated BK (1 μg into the LA) induced consistent discharge activity in six separate afferents. We then observed that the coadministration of U-46619 (5 μg) and BK (1 μg into the LA) together caused a total response that was significantly higher than the predicted response by the simple addition of the individual responses. BK (1 μg) facilitated eight cardiac afferent responses to U-46619 (5 μg into the LA) by 64%. In contrast, repeated U-46619 (5 μg into the LA) without intervening BK stimulation evoked consistent responses in seven other ischemically sensitive afferents. Finally, inhibition of cyclooxygenase with indomethacin (5 mg/kg iv) eliminated the potentiating effects of BK on the cardiac afferent response to U-46619 (5 μg into the LA) but did not alter the afferent response to U-46619. These data suggest that BK and TxA2 reciprocally interact to stimulate ischemically sensitive cardiac afferent endings leading to synergistic afferent responses and that the BK sensitization effect is mediated by cyclooxygenase products.

Vagal afferent and reflex responses to changes in surface osmolarity in lower airways of dogs

1992 ◽  
Vol 73 (6) ◽  
pp. 2305-2313 ◽  
Author(s):  
T. E. Pisarri ◽  
A. Jonzon ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Evaporative Water ◽  
Lung Lobe ◽  
C Fibers ◽  
Lobar Bronchus ◽  
Shallow Breathing ◽  
Afferent Vagal ◽  
Lower Airways ◽  
Exercise Induced

In anesthetized dogs we examined the sensitivity of afferent vagal endings in the lungs to changes in airway fluid osmolarity. Injection of 0.25–0.5 ml/kg water or hyperosmotic sodium chloride solutions (1,200–2,400 mmol/l) into a lobar bronchus caused bradycardia, arterial hypotension, apnea followed by rapid shallow breathing, and contraction of tracheal smooth muscle. All effects were abolished by vagotomy. We examined the sensory mechanisms initiating these effects by recording afferent vagal impulses arising from the lung lobe into which the liquids were injected. Water stimulated pulmonary and bronchial C-fibers and rapidly adapting receptors; isosmotic saline and glucose solutions were ineffective. Hyperosmotic saline (1,200–9,600 mmol/l, 0.25–1 ml/kg) stimulated these afferents in a concentration-dependent manner. Stimulation began 1–10 s after the injection and sometimes continued for several minutes. Responses of slowly adapting stretch receptors varied. Our results suggest that non-isosmotic fluid in the lower airways initiates defense reflexes by stimulating pulmonary and bronchial C-fibers and rapidly adapting receptors. Conceivably, stimulation of these afferents as a result of evaporative water loss from airway surface liquid could contribute to exercise-induced asthma.

scholarly journals Assessment of Behavioral Disruption in Rats with Abdominal Inflammation Using Visual Cue Titration and the Five-choice Serial-reaction Time Task

2017 ◽  
Vol 127 (2) ◽  
pp. 372-381 ◽  
Author(s):  
Thomas J. Martin ◽  
Tracy J. Strassburg ◽  
Amanda L. Grigg ◽  
Susy A. Kim ◽  
Douglas G. Ririe ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Visual Attention ◽  
Intraperitoneal Administration ◽  
Reaction Time Task ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Impaired Performance ◽  
Operant Task ◽  
The Impact ◽  
Dose Dependent

Abstract Background Both acute and chronic pain result in a number of behavioral symptoms in patients, including cognitive effects such as decreased attention and working memory. Intraperitoneal administration of dilute lactic acid in rodents has been used to induce abdominal inflammation and produce effects in behavioral assays of both sensory-discriminative and affective pain modalities. Methods Intraperitoneal injection of dilute lactic acid was used to study the impact of abdominal inflammation on an operant task requiring sustained visual attention in rats (N = 7 to 15/group) that adapts dynamically to performance ability. The effects of ketoprofen and morphine on lactic acid–induced impairment were compared with those on the disruptive effects of scopolamine. Results Lactic acid impaired performance in a concentration-dependent manner, increasing the duration of cue presentation required to maintain optimal performance from 0.5 ± 0.2 s (mean ± SD) to 17.2 ± 11.4 s after the administration of 1.8% (v/v) (N = 13). The latency to emit correct responses and to retrieve the food reward were both increased by lactic acid. All effects of lactic acid injection were reversed by both ketoprofen and morphine in a dose-dependent manner. Scopolamine, however, produced dose-dependent, nonpain-related disruption in sustained attention that was not altered by either ketoprofen or morphine. Conclusions These data demonstrate that abdominal inflammation induced by lactic acid produces robust disruption in a visual attention-based operant task and that this disruption is reversed by analgesics. Future studies will focus on pain-related circuitry and its impact on both limbic forebrain and frontal cortical mechanisms.

Fentanyl decreases discharges of C and A nociceptors to suprathreshold mechanical stimulation in chronic inflammation

2012 ◽  
Vol 108 (10) ◽  
pp. 2827-2836 ◽  
Author(s):  
Rabih Moshourab ◽  
Christoph Stein
Keyword(s):  
Chronic Inflammation ◽  
Tissue Injury ◽  
Mechanical Hyperalgesia ◽  
Acute Injury ◽  
Dependent Manner ◽  
Mechanical Stimuli ◽  
Nociceptive Neurons ◽  
C Fibers ◽  
C Fiber ◽  
Inflamed Tissue

An essential component of mechanical hyperalgesia resulting from tissue injury is an enhanced excitability of nociceptive neurons, termed mechanical sensitization. Local application of opioids to inflamed rat paws attenuates mechanical hyperalgesia and reduces electrical excitability of C-fiber nociceptors in acute injury. Here, we examined the effects of the opioid receptor agonist fentanyl on the mechanical coding properties of not only C- but also A-fiber nociceptors innervating the rat hind paw in a model of chronic pain, i.e., 4 days after Freund's complete adjuvant-induced inflammation. The peripheral mechanosensitive terminals of C-fibers ( n = 143), A-fibers ( n = 79), and low-threshold mechanoreceptors ( n = 25) were characterized using the in vitro skin-nerve preparation from the saphenous nerve. Although mechanical activation thresholds were not changed, discharges to suprathreshold mechanical stimuli were elevated significantly in both A- and C-fiber nociceptors from inflamed tissue. In addition, the proportion of nociceptors as well as the frequency of spontaneous discharges in A (14% vs. 0%)- and C (28% vs. 8%)-fibers were increased in inflamed compared with normal tissue. Fentanyl inhibited responses to suprathreshold stimuli in a significantly higher proportion of not only C (36% vs. 7%)- but also A (41% vs. 8%)-fibers in inflamed tissue in a naloxone-reversible and concentration-dependent manner. Our results demonstrate that mechanical sensitization persists in chronic inflammation, in correlation with behavioral hyperalgesia. Opioid sensitivity of both A- and C-fibers is markedly augmented. This is consistent with an upregulation or enhanced functionality of opioid receptors located at the peripheral terminals of sensitized nociceptors.

The Anti-Atherogenic Properties of Sesamin are Mediated via Improved Macrophage Cholesterol Efflux Through PPARγ1-LXRα and MAPK Signaling

2014 ◽  
Vol 84 (1-2) ◽  
pp. 79-91 ◽  
Author(s):  
Amin F. Majdalawieh ◽  
Hyo-Sung Ro
Keyword(s):  
Cholesterol Efflux ◽  
Transcriptional Activity ◽  
Molecular Mechanisms ◽  
Foam Cell ◽  
Mapk Signaling ◽  
Luciferase Reporter ◽  
Foam Cell Formation ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Macrophage Cholesterol Efflux

Background: Foam cell formation resulting from disrupted macrophage cholesterol efflux, which is triggered by PPARγ1 and LXRα, is a hallmark of atherosclerosis. Sesamin and sesame oil exert anti-atherogenic effects in vivo. However, the exact molecular mechanisms underlying such effects are not fully understood. Aim: This study examines the potential effects of sesamin (0, 25, 50, 75, 100 μM) on PPARγ1 and LXRα expression and transcriptional activity as well as macrophage cholesterol efflux. Methods: PPARγ1 and LXRα expression and transcriptional activity are assessed by luciferase reporter assays. Macrophage cholesterol efflux is evaluated by ApoAI-specific cholesterol efflux assays. Results: The 50 μM, 75 μM, and 100 μM concentrations of sesamin up-regulated the expression of PPARγ1 (p< 0.001, p < 0.001, p < 0.001, respectively) and LXRα (p = 0.002, p < 0.001, p < 0.001, respectively) in a concentration-dependent manner. Moreover, 75 μM and 100 μM concentrations of sesamin led to 5.2-fold (p < 0.001) and 6.0-fold (p<0.001) increases in PPAR transcriptional activity and 3.9-fold (p< 0.001) and 4.2-fold (p < 0.001) increases in LXR transcriptional activity, respectively, in a concentration- and time-dependent manner via MAPK signaling. Consistently, 50 μM, 75 μM, and 100 μM concentrations of sesamin improved macrophage cholesterol efflux by 2.7-fold (p < 0.001), 4.2-fold (p < 0.001), and 4.2-fold (p < 0.001), respectively, via MAPK signaling. Conclusion: Our findings shed light on the molecular mechanism(s) underlying sesamin’s anti-atherogenic effects, which seem to be due, at least in part, to its ability to up-regulate PPARγ1 and LXRα expression and transcriptional activity, improving macrophage cholesterol efflux. We anticipate that sesamin may be used as a therapeutic agent for treating atherosclerosis.

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