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Danshen-Chuanxiong-Honghua ameliorates neurological function and inflammation in traumatic brain injury in rats via modulating Ghrelin/GHSR.
J Ethnopharmacol
Xiaohang Zhang, Yawen Cai, Meng Chen +7 more
Guanxin II, proposed by Chen Keji (National master of traditional Chinese medicine), possesses neuroprotective effect. Interestingly, its simplified prescription Danshen-Chuanxiong-Honghua (DCH) can also clinically ameliorate cerebral impairment and improve spatial cognitive deficits, similar to the function of original formula.
Neuroimmune mechanisms of type 2 inflammation in the skin and lung.
Allergol Int
Masato Tamari, Aaron M Ver Heul
Type 2 inflammation has a major role in barrier tissues such as the skin and airways and underlies common conditions including atopic dermatitis (AD) and asthma. Cytokines including interleukin 4 (IL-4), IL-5, and IL-13 are key immune signatures of type 2 inflammation and are the targets of multiple specific therapeutics for allergic diseases. Despite shared core immune mechanisms, the distinct structures and functions of the skin and airways lead to unique therapeutic responses. It is increasingly recognized that the nervous system has a major role in sensing and directing inflammatory processes. Indeed, crosstalk between type 2 immune activation and somatosensory functions mediates tissue-specific signatures such as itching in the skin. However, neuroimmune interactions are shaped by distinct neuronal and immune landscapes, and differ between the skin and airways. In the skin, dorsal root ganglia-derived neurons mediate pruritus via type 2 cytokines and neurogenic inflammation by mast cell or basophil activation. Conversely, vagal ganglia-derived neurons regulate airway immune responses by releasing neuropeptides/neurotransmitters such as calcitonin gene-related peptides, neuromedin U, acetylcholine, and noradrenaline. Sensory neuron-derived vasoactive intestinal peptide forms a feedback loop with IL-5, amplifying eosinophilic inflammation in the airways, a mechanism that is absent in the skin. These differences influence the efficacy of cytokine-targeted therapies. For instance, IL-4/IL-13-targeted therapies like dupilumab demonstrate efficacy in AD and allergic airway diseases, whereas IL-5-targeted therapies are effective in eosinophilic asthma but not AD. Understanding these neuroimmune interactions underscores the need for tailored therapeutic approaches to address allergic diseases where barrier tissues are involved.
Vasoactive Intestinal Peptide: A Neuropeptide that Plays an Important Role in Parkinson's Disease.
Curr Neuropharmacol
Wenhui Fan, Ke Li, Ruohua Wang +5 more
Parkinson's disease (PD) is primarily characterized by rigidity and tremor, which are pathologically associated with α -synuclein aggregation, especially in dopaminergic neurons in the midbrain. As it is a multi-factorial disease, there are currently no effective treatments but only mitigative therapies. Vasoactive intestinal peptide (VIP), a 28-amino acid neurotransmitter, is widely distributed in both the central and peripheral nervous system with a broad biological effect. Studies have shown that VIP exhibits anti-inflammatory, antioxidant, and anti-apoptotic effects and regulates glial cells and immune cells to protect and repair nerve cells. This article reviews the research progress of VIP as a brain-gut peptide in the treatment of PD and possible future research directions.
Spatial regulation of mitochondrial membrane potential by α5β1 integrin engagement in collective cell migration.
J Cell Sci
Gustavo G Pacheco, Bette J Dzamba, Wakako Endo +9 more
The mechanistic links between mechanical forces and bioenergetics remain elusive. We report an increase in mitochondrial membrane potential (MMP) along the leading row of collectively migrating Xenopus laevis mesendoderm cells at sites where fibronectin-α5β1 integrin substrate traction stresses are greatest. Real-time metabolic analyses reveal α5β1 integrin-dependent increases in respiration efficiency in cells on fibronectin substrates. Elevation of metabolic activity is reduced following pharmacologic inhibition of focal adhesion kinase (FAK; also known as PTK2) signaling. Attachment of mesendoderm cells to fibronectin fragments that support differing α5β1 integrin conformational and ligand-binding affinity states, increases MMP when both the Arg-Gly-Asp (RGD) and Pro-Pro-Ser-Arg-Asn (PPSRN) synergy sites of fibronectin are engaged by the receptor. Cell stretch on deformable fibronectin substrates also results in a FAK-dependent increase in MMP. Inhibition of MMP or ATP-synthase activity slows collective cell migration velocity in vivo, further suggesting that integrin-dependent adhesion and signaling contribute to metabolic changes. These data highlight an underexplored link between extracellular matrix (ECM)-integrin adhesion and metabolic activity in embryonic cell migration. We propose that fibronectin-integrin adhesion and signaling help shape the metabolic landscape of collectively migrating cells.
GLP-1 and ghrelin inversely regulate insulin secretion and action in pancreatic islets, vagal afferents, and hypothalamus for controlling glycemia and feeding.
Am J Physiol Cell Physiol
Toshihiko Yada, Katsuya Dezaki, Yusaku Iwasaki
Glucagon-like peptide-1 (GLP-1) was discovered as an incretin hormone, which is released from the intestine upon nutrient intake and stimulates insulin secretion from the pancreatic islet β-cells. Subsequently, its ability to suppress appetite was recognized. Ghrelin, discovered as the ligand for growth hormone secretagogue-receptor (GHS-R), is released from the stomach and produces appetite. Later, its ability to inhibit insulin secretion and elevate blood glucose was found. Thus, GLP-1 and ghrelin regulate insulin secretion and appetite toward opposite directions. The receptor agonists for GLP-1 and ghrelin have been developed and are now used to treat metabolic diseases, in which insulin plays a key role. However, underlying action mechanism and possible interplay of these hormones have remained elusive. Here, we describe that GLP-1 and ghrelin reciprocally regulate the insulin system. GLP-1 enhances and ghrelin suppresses insulin secretion in pancreatic β-cells. Moreover, GLP-1 cooperates with and ghrelin counteracts insulin action in the vagal afferent and hypothalamic arcuate nucleus (ARC) neurons, the interfaces between the peripheral metabolism and brain. Notably, ghrelin rises and works preprandially and GLP-1 rises and works postprandially. The interplay of ghrelin, GLP-1, and insulin leads to optimal circadian control of feeding, glycemia, and metabolism.
Prebiotics pectin and resistant starch-type 4 stimulate peptide YY and cholecystokinin to promote satiety, and improve gut microbiota composition.
FASEB J
Souvik Patra, Savana L Everhart Nunn, Gizem Levent +1 more
Dietary prebiotics pectin and resistant starch type-4 (RS-4) promote satiety and alter gut microbiota; however, the underlying neurohormonal mechanisms of satiety remain poorly understood. We determined the effects of pectin, RS-4, and their combination on energy balance and gut microbiota composition, and assessed whether the gut hormones peptide YY (PYY) and cholecystokinin (CCK) play a role in fiber-induced satiety. High-fat diet -induced obese male rats (n = 7-8/group) were fed either control, pectin, RS-4, or a combination of pectin and RS-4 diet. We found that pectin, RS-4, and their combination decreased food intake. Pectin alone, or combined with RS-4, shifted substrate utilization towards fat and reduced gains in weight and adiposity. Pectin alone or combined with RS-4 enhanced the expression and plasma concentrations of PYY and CCK. Importantly, systemic blockade of PYY-Y2 and CCK-1 receptors attenuated the hypophagic effects of pectin, and CCK-1 receptor blockade partly attenuated the hypophagia from RS-4. The prebiotics significantly altered fecal β-diversity metrics, suggestive of improvements in gut microbiota composition. Pectin and RS-4 alone, or in combination, were associated with increased relative abundance of phylum Bacteroidota, decreased Firmicutes, and increased concentrations of amino acids and biogenic amines in feces. Collectively, these findings suggest that dietary pectin and RS-4 improved energy balance and gut microbiota composition, and importantly, demonstrated that the satiety effects of these diets were mediated, in part, via enhanced endogenous PYY and CCK signaling.
Subchronic safety assessment of CIGB-500 in beagle dog after repeated daily dose administration over 28 days.
Regul Toxicol Pharmacol
Jorge Castro, Imran Shaikh, Sherwin Silo +9 more
CIGB-500 is a product whose active pharmaceutical ingredient is GHRP-6, (Growth Hormone Releasing Peptide-6), a synthetic peptide that allows the rescue of cardiac mass affected during Acute Myocardial Infarction. The objective of the study was to determine the toxicity profile of CIGB-500 in dogs. As general methodology, CIGB-500 was administered daily to dogs by intravenous route for 28 consecutive days. All animals were allocated to four groups: Control, Low-Dose (300 μg/kg/day), Mid dose (1000 μg/kg/day) and High-Dose (2000 μg/μg/day). Hypersalivation, hypoactivity, reduced heart rate, changes in respiration, pale gums and erythema of the head region were observed in some animals administered at 1000 and 2000 μg/kg/day. These clinical signs were transient, and were therefore considered non-adverse. Treatment with CIGB-500 did not result in any adverse macroscopic or microscopic changes. A decrease in heart rate value was noted following CIGB-500 treatment at all dose levels an at the end of recovery period, the heart rate effects at 2000 μg/kg/day were comparable to controls. In conclusion, the daily administration of CIGB-500 at doses up to 2000 μg/kg/day was well-tolerated, findings noted were transient, minor, non-adverse and reversible, and the no observable adverse effect level (NOAEL) was considered to be 2000 μg/kg/day.
Oxytocin improves maternal licking behavior deficits in autism-associated Shank3 mutant dogs.
Transl Psychiatry
Wen Lyu, Yuan Li, Aiyu Yao +7 more
Impaired social interaction and repetitive behavior are key features observed in individuals with autism spectrum disorder (ASD). SHANK3 is a high-confidence ASD risk gene that encodes an abundant scaffolding protein in the postsynaptic density. In wild-type (WT) domestic dogs, maternal behaviors such as licking and nursing (largely milk feeding) of puppies are most commonly observed. To address whether SHANK3 plays a role in social behaviors especially maternal behaviors, we analyzed Shank3 mutant dogs generated by CRISPR/Cas9 methodology. We found that Shank3 mutant dams exhibited a fewer and shorter licking behavior, as well as reduced nursing frequency when compared with WT dams. Additionally, a significant decrease in blood oxytocin (OXT) concentration was detected in Shank3 mutant dams. We thus conducted a vehicle-controlled experiment to examine whether a two-week intranasal OXT treatment, initiated on the 8th postpartum day, could rescue the maternal licking deficits in Shank3 mutant dams. We found that the decreased licking behavior in Shank3 mutant dams was significantly attenuated both acutely and chronically by OXT treatment. The rescue effect of OXT implicates an oxytocinergic contribution to the maternal defects in Shank3 mutant dams, suggesting a potential therapeutic strategy for SHANK3-associated ASD.
Nanoscale distribution of bioactive ligands on biomaterials regulates cell mechanosensing through translocation of actin into the nucleus.
Proc Natl Acad Sci U S A
Xiaojing Liu, Man Zhang, Peng Wang +8 more
Cells respond to adhesive ligands such as arginine-glycine-aspartate (RGD) through integrins, which regulates cellular activities via influencing cytoskeleton assembly. Herein, we report that the nanoscale distribution of active ligands on biomaterials regulates cells through not only cytoplasmic tension but also nuclear tension. This is particularly related to translocation of actin into nucleus and highlighted in our interpretation of an "abnormal" phenomenon that large RGD nanospacing (>70 nm) disassembles integrin clusters, inhibits cell adhesion, but promotes osteogenic differentiation of mesenchymal stem cells. Our studies reveal that the unstable adhesion at the 150 nm RGD distance increases actin dynamics, resulting in the nuclear translocation of globular (G) actin. The compartment polymerization of more G-actins to filamentous actins in nucleus increases nuclear tension, facilitating transcription activity and releasing calcium ions from the endoplasmic reticulum. This noncanonical mechanotransduction process sheds insight into mechanotransduction pertinent to cell-material interactions.
Protective Effects of BPC 157 on Liver, Kidney, and Lung Distant Organ Damage in Rats with Experimental Lower-Extremity Ischemia-Reperfusion Injury.
Medicina (Kaunas)
Hüseyin Demirtaş, Abdullah Özer, Alperen Kutay Yıldırım +3 more
Background and Objectives: Ischemia-reperfusion (I/R) injury can affect multiple distant organs following I/R in the lower extremities. BPC-157's anti-inflammatory and free radical-neutralizing properties suggest its potential in mitigating ischemia-reperfusion damage. This study evaluates the protective effects of BPC-157 on remote organ damage, including the kidneys, liver, and lungs, in a rat model of skeletal muscle I/R injury. Materials and Methods: A total of 24 male Wistar albino rats were randomly divided into four groups: sham (S), BPC-157(B), lower extremity I/R(IR) and lower extremity I/R+BPC-157(I/RB). Some 45 min of ischemia of lower extremity was followed by 2 h of reperfusion of limbs. BPC-157 was applied to groups B and I/RB at the beginning of the procedure. After 2 h of reperfusion, liver, kidney and lung tissues were harvested for biochemical and histopathological analyses. Results: In the histopathological examination, vascular and glomerular vacuolization, tubular dilation, hyaline casts, and tubular cell shedding in renal tissue were significantly lower in the I/RB group compared to other groups. Lung tissue showed reduced interstitial edema, alveolar congestion, and total damage scores in the I/RB group. Similarly, in liver tissue, sinusoidal dilation, necrotic cells, and mononuclear cell infiltration were significantly lower in the I/RB group. Additionally, the evaluation of TAS, TOS, OSI, and PON-1 revealed a statistically significant increase in antioxidant activity in the liver, lung, and kidney tissues of the I/RB group. Conclusions: The findings of this study demonstrate that BPC-157 exerts a significant protective effect against distant organ damage in the liver, kidneys, and lungs following lower extremity ischemia-reperfusion injury in rats.
Self-Assembled Peptide-Gold Nanoparticle 1D Nanohybrids Functionalized with GHK Tripeptide for Enhanced Wound-Healing and Photothermal Therapy.
ACS Appl Mater Interfaces
Nayeong Jeon, Leeseo Kim, Seong Gyu Choi +5 more
Glycyl-l-histidyl-l-lysine (GHK) tripeptides are known for their remarkable therapeutic potential, including wound-healing, anti-inflammatory activity, and cellular regeneration. However, their clinical application has been significantly hindered by poor biological stability and limited efficacy in a physiological medium. In this study, we introduce a sophisticated approach to overcome these limitations by developing supramolecular peptide nanofiber-gold (Au) nanoparticle (NP) hybrids functionalized with GHK tripeptides. By strategically manipulating peptide self-assembly and NP integration, we demonstrated a useful platform that enhances both therapeutic efficacy and material stability. Our methodology involves the precise engineering of 9-fluorenylmethoxycarbonyl-diphenylalanine scaffolds with GHK and KHG tripeptides, enabling robust nanofibril formation through π-π stacking and hydrogen bonding. Critically, we discovered that the specific amino acid sequence significantly influences the surface exposure of lysine, directly impacting the nanohybrid's wound-healing capabilities. The resultant nanohybrids exhibit exceptional characteristics: Au NPs are spatially confined within the peptide nanofibers, achieving a remarkably uniform size distribution of approximately 3 nm. These nanohybrids demonstrate superior near-infrared (NIR) light absorption and photothermal conversion efficiency, enabling effective eradication of cancer cells and organoids killing under NIR irradiation. This dual-functional nanohybrid integrates biocompatible and enzymatically degradable peptide scaffolds to achieve synergistic wound-healing and cancer-killing effects. By mitigating the cytotoxicity and biodegradability issues associated with conventional photothermal agents, our system provides a promising strategy to improve postoperative cancer therapy and promote tissue regeneration. This work highlights the potential of peptide-inorganic nanohybrids in advancing multifunctional therapeutic platforms for cancer treatment and tissue repair.
Cisplatin-Induced Muscle Wasting and Atrophy: Molecular Mechanism and Potential Therapeutic Interventions.
J Cachexia Sarcopenia Muscle
Ko-Chieh Huang, Yi-Fen Chiang, Mohamed Ali +1 more
Platinum-based chemotherapeutics, particularly cisplatin, are crucial in the treatment of various malignancies due to their strong antitumor effects. However, a significant side effect of cisplatin is muscle atrophy, which severely impairs physical strength, diminishes quality of life and complicates cancer therapy. Cisplatin-induced muscle wasting arises from a complex interplay of enhanced proteolysis, reduced muscle protein synthesis and systemic inflammation. Understanding the underlying molecular mechanisms of muscle atrophy is vital for identifying new therapeutic targets. This review systematically explores molecular-based therapies and plant-derived natural compounds, providing a comprehensive overview of their efficacy in vivo and in vitro for preventing cisplatin-induced muscle atrophy. Both molecular-based therapies and plant-derived natural compounds present promising strategies for mitigating cisplatin-induced muscle atrophy. Ghrelin, growth hormone secretagogues and testosterone stimulate anabolic pathways and reduce muscle degradation, whereas natural compounds like capsaicin and naringenin exert protective effects by reducing inflammation and oxidative stress. A better understanding of the pathophysiology of muscle atrophy, combined with optimized therapeutic applications, may facilitate the clinical translation of these interventions to improve outcomes for cancer patients undergoing chemotherapy.
Assessment of skeletal muscle alterations and circulating myokines in metabolic dysfunction-associated steatotic liver disease: A cross-sectional study.
World J Gastroenterol
Yolanda Real Martinez, Carlos Ernesto Fernandez-Garcia, Esther Fuertes-Yebra +11 more
Skeletal muscle alterations (SMAs) are being increasingly recognized in patients with metabolic dysfunction-associated steatotic liver disease (MASLD) and appear to be associated with deleterious outcomes in these patients. However, their actual prevalence and pathophysiology remain to be elucidated.
Detection of chimeric alpha-defensin transcripts and peptides in mouse Paneth cells.
Front Immunol
Steven Timmermans, Charlotte Wallaeys, Somara De Beul +2 more
In mammals, Paneth cells, located in the crypts of the small intestine, produceantimicrobial peptides that serve to keep the intestinal microbiome under control. a-Defensins are the primary antimicrobial peptides produced by these cells.
Exploring the therapeutic potential of MOTS-c in age-related macular degeneration: from cellular responses to patient-derived cybrids.
Hum Cell
Zahra Mohtashami, Kevin Schneider, Reza Azimi +4 more
Age-related macular degeneration (AMD), the leading cause of irreversible vision loss in the US, is on the rise among the elderly. Uncontrolled mitochondria-derived peptide production from mtDNA disruption and 16S or 12S rRNA damage could worsen AMD. Our previous work has shown that Humanin G possesses cytoprotective effects in retinal pigment epithelial (RPE) cells. However, MOTS-c, a highly efficient mitochondrial peptide, has yet to be evaluated on retinal cell survival. In this study, we show that there are differences in effects between wild-type (wt-) and differentiated ARPE19 cells (diff-ARPE19), implying that the cellular differentiation status may influence how cells respond to MOTS-c. MOTS-c has dose-dependent effects on apoptosis, inflammation, and mitochondrial biogenesis in diff-ARPE19 cells. Lower doses (500 nM) have more significant impacts than 5 µM concentrations. In diff-ARPE19 cells, a lower dose of MOTS-c can reduce the negative impact of hypoxia on cellular survival and gene expression, including apoptosis (CASP3, CASP9), mitochondrial biogenesis (TFAM, PGC-1α), and metabolic sensor (AMPK). However, it had no significant effect on ROS levels or NRF1 expression, regardless of MOTS-c dose. Exposing diff-ARPE19 cells to varied MOTS-c dosages before and after therapy in a chemically induced hypoxic environment yields no extra benefits as compared to MOTS-c treatment alone. MOTS-c had different effects on the expression of genes linked with apoptosis, mitochondrial biogenesis, and antioxidant activity in AMD patients versus age-matched control cybrids. The MOTS-c peptide appears to enhance cellular metabolism and regulate gene expression, which could potentially provide therapeutic benefits in AMD.
Exploring the Relationship Between Thymosin β4 Protein and First Myocardial Infarction on the Basis of Proteomics.
J Am Heart Assoc
Ziyu Lu, Qinghua Liu, Yonghua Fan +3 more
Plasma protein alterations may occur in patients with acute myocardial infarction (AMI). In this study, we investigated the plasma proteomics of patients with first-onset AMI to identify a novel diagnostic target for myocardial infarction.
Proinflammatory cytokines and neuropeptides in psoriasis, depression, and anxiety.
Acta Physiol (Oxf)
Emily L Keenan, Richard D Granstein
Psoriasis vulgaris has established associations with psychiatric conditions such as depression, anxiety, and chronic stress. This review aims to evaluate current theories and evidence regarding the role of proinflammatory cytokines and neuropeptides in connecting systemic inflammation, psychological stress, and inflammatory skin diseases, namely psoriasis. A literature review was conducted to analyze studies that explore the connections between psoriasis, psychiatric conditions, and biological mediators, including inflammatory cytokines [interferon (IFN)-γ, interleukin (IL)-1, IL-2, IL-6, IL-12, tumor necrosis factor (TNF)-α, IL-22, IL-17], neuropeptides [calcitonin gene-related peptide (CGRP), substance P (SP), and vasoactive intestinal peptide (VIP)], as well as the hypothalamic-pituitary-adrenal (HPA) axis. Existing literature indicates that psychiatric state can influence cutaneous conditions through immune, neural, and endocrine mediators. The elevated rates of anxiety and depression observed in psoriasis patients are likely due to both the inflammatory process itself and the chronic stress associated with disease management, highlighting the importance of managing stress, and addressing mental health to improve clinical outcomes. While the literature suggests proinflammatory cytokines and neuropeptides may be key links between systemic inflammation, psoriasis, and psychiatric comorbidities, further research is necessary to continue to elucidate physiological mechanisms and explore the potential for new treatment modalities.
GDF11 alleviates cardiac ischemia/reperfusion injury by suppressing the mtDNA damage-inflammatory response axis.
Eur J Pharmacol
Dan Zhao, Zihui Wang, Yanyan Chen +8 more
Growth differentiation factor 11 (GDF11) has been reported to play a protective role in myocardial infarction. Mitochondrial DNA (mtDNA) damage is one of the pivotal factors in the initiation of myocardial cell damage. However, whether GDF11 can ameliorate mtDNA damage through its cardioprotective effect remains largely unknown. In this study, we obtained the GDF11-Fc fusion protein from mammalian cells and evaluated its cardioprotective effect in a mouse myocardial infarction model by TTC-Evans blue staining and morphological and enzymatic detection. Similar protective effects were observed in H9C2 cells and NRVMs. Mechanistically, we found that mtDNA damage was increased in I/R hearts. Exogenous administration of GDF11-Fc alleviated mtDNA damage and subsequent NLRP3 inflammasome activity, possibly through a reduction in ROS. In conclusion, GDF11 can ameliorate myocardial ischemia-reperfusion injury by inhibiting the inflammatory response induced by mtDNA damage.
Elamipretide: A Review of Its Structure, Mechanism of Action, and Therapeutic Potential.
Int J Mol Sci
Cheryl Tung, Fahimeh Varzideh, Emanuele Farroni +4 more
Mitochondria serve an essential metabolic and energetic role in cellular activity, and their dysfunction has been implicated in a wide range of disorders, including cardiovascular conditions, neurodegenerative disorders, and metabolic syndromes. Mitochondria-targeted therapies, such as Elamipretide (SS-31, MTP-131, Bendavia), have consequently emerged as a topic of scientific and clinical interest. Elamipretide has a unique structure allowing for uptake in a variety of cell types and highly selective mitochondrial targeting. This mitochondria-targeting tetrapeptide selectively binds cardiolipin (CL), a lipid found in the inner mitochondrial membrane, thus stabilizing mitochondrial cristae structure, reducing oxidative stress, and enhancing adenosine triphosphate (ATP) production. Preclinical studies have demonstrated the protective and restorative efficacy of Elamipretide in models of heart failure, neurodegeneration, ischemia-reperfusion injury, metabolic syndromes, and muscle atrophy and weakness. Clinical trials such as PROGRESS-HF, TAZPOWER, MMPOWER-3, and ReCLAIM elaborate on preclinical findings and highlight the significant therapeutic potential of Elamipretide. Further research may expand its application to other diseases involving mitochondrial dysfunction as well as investigate long-term efficacy and safety of the drug. The following review synthesizes current knowledge of the structure, mechanisms of action, and the promising therapeutic role of Elamipretide in stabilizing mitochondrial fitness, improving mitochondrial bioenergetics, and minimizing oxidative stress.
Thymosin β4 Regulates Tissue Inflammatory Response in Mouse Nonalcoholic Fatty Liver Disease by Promoting Macrophage M2-Type Polarization.
J Inflamm Res
Zixin Zhu, Yifan Liao, Qiuju Mou +4 more
Nonalcoholic fatty liver disease (NAFLD) is characterized by hepatic steatosis, insulin resistance, and systemic pro-inflammatory response. Thymosin β4 (Tβ4) is a bioactive polypeptide that inhibits extracellular matrix (ECM) deposition and protects the liver. It can achieve immune homeostasis by regulating the polarization of liver macrophages and is a potential treatment for NAFLD.