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Mechanistic study of the Tβ4/SLC7A11 signaling pathway regulating breast cancer evolution.
Cell Signal
Zhaoyan Jin, Hongshu Li, Jiafeng Li +4 more
Thymosin β4 (Tβ4) plays a critical role in breast cancer progression, yet its molecular mechanism remains unclear. In this study, we identified that Tβ4 is significantly upregulated in breast cancer tissues and cell lines, and its high expression correlates with poor clinical outcomes. Functionally, Tβ4 promotes breast cancer cell proliferation, migration, epithelial-mesenchymal transition (EMT), and angiogenesis while inhibiting apoptosis. Mechanistically, Tβ4 directly regulates the expression of SLC7A11, a key cystine/glutamate antiporter, thereby enhancing glutathione biosynthesis and suppressing lipid peroxidation to inhibit ferroptosis. Rescue experiments further demonstrated that silencing SLC7A11 abrogates the oncogenic effects of Tβ4 both in vitro and in vivo. Collectively, these findings uncover a novel Tβ4/SLC7A11 axis that modulates ferroptosis sensitivity and contributes to breast cancer malignancy, offering potential therapeutic implications for targeting ferroptosis resistance.
Aza-Isotryptophan: Synthesis, Pictet-Spengler Chemistry, Incorporation and Conformational Analysis in Peptides, and Activity in Modulators of the Cluster of Differentiation-36 Receptor.
J Med Chem
Xiaozheng Wei, Mukandila Mulumba, Sylvain Chemtob +2 more
Isotryptophan (Itr) is the rare 2-indoyl counterpart of the essential amino acid tryptophan. Considering the potential to explore novel side chain χ-space in a residue prone to adopt backbone turn conformers, azaItr has been effectively synthesized and employed in Pictet-Spengler and peptide chemistry. β-Turn geometry was characterized in model peptides of the Ala-azaItr-d-Phe triad by X-ray and NMR analyses. Moreover, azaItr analogs of growth hormone-releasing peptide 6 (GHRP-6) demonstrated a promising cluster of differentiation-36 receptor (CD36) binding affinity and modulatory effect on the inflammatory response induced by the activated complex composed of the latter coreceptor in the Toll-like receptor-2/6 heterodimer.
Impact of GHRL (RS696217) and LEPR (RS1137101) gene polymorphisms on hormonal and anthropometric outcomes after bariatric surgery.
Endocr Regul
Andrii Prodan
Objective. The aim of the study was to evaluate the influence of GHRL (rs696217) and LEPR (rs1137101) gene polymorphisms on weight loss dynamics and endocrine marker changes following various bariatric procedures. Patients and Methods. A total of 76 patients undergoing laparoscopic sleeve gastrectomy (LSG), gastric plication (LGCP), and gastric artery embolization (GAE) were genotyped for GHRL (rs696217) and LEPR (rs1137101). Body mass index (BMI), total weight loss (TWL), excess weight loss (EWL), and hormonal markers (ghrelin, leptin, adiponectin, resistin, HbA1c) were assessed preoperatively and at 3, 6, and 12 months postoperatively. Results. Carriers of the T allele of GHRL (rs696217) experienced significantly greater reductions in BMI, TWL, and EWL, particularly following LSG and GAE (p<0.05). A notable reduction in total ghrelin levels was observed in T allele carriers (up to -46.75%, p<0.001) 6 months after surgery. Improvements in resistin (p=0.0002) and HbA1c (p=0.014) levels were also more pronounced in this group. LEPR (rs1137101) polymorphism showed limited impact on outcomes after LGCP, but it was associated with improved TWL and EWL in A allele carriers after LSG (p=0.006 and p=0.016, respectively). Conclusion. The T allele of GHRL (rs696217) appears to be a promising predictive marker for greater metabolic and hormonal improvement following bariatric procedures targeting the ghrelin-producing stomach zones. LEPR (rs1137101) may also influence postoperative outcomes in a procedure-specific manner. These findings support the potential role of genetic screening in optimizing patient selection and predicting surgical success.
Effects of Long-term low-dose intermittent rapamycin administration on glucose metabolism and immune system of SAMP8 and SAMR1 mice.
Front Immunol
Luiz Adriano Damasceno Queiroz, Rafael Santos Barros, Josiane Betim Assis +6 more
Aging involves a gradual decline in physiological integrity, and rapamycin (RAPA) has demonstrated potential as an anti-aging agent. Nonetheless, its effects on glucose metabolism and immune function may vary based on dosage and administration regimen. This study investigates the impact of intermittent low-dose RAPA on glucose metabolism and immune function in Senescence-Accelerated Mouse Prone 8 (SAMP8) and Senescence-Accelerated Mouse Resistant 1 (SAMR1) mice. Twelve-week-old male SAMP8 and SAMR1 mice were treated with RAPA (0.78 µg/kg) every five days for six months. Glucose uptake, mitochondrial respiratory capacity, spleen and thymus immunophenotype, lymphoproliferation, and cytokine profiles were evaluated. Our findings indicate that RAPA reduced glucose uptake in the bladder and the percentage of FoxP3+ lymphocytes in the spleen of SAMP8 mice, while enhancing mitochondrial respiratory control and ATP production in liver. In SAMR1 mice, RAPA administration led to a decrease in CD3+ thymocytes and splenic lymphoproliferative capacity, while also enhanced mitochondrial performance. Comparisons between Control groups revealed that SAMP8 mice exhibited higher glucose uptake in several tissues, lower lymphocyte populations in spleen and thymus, altered CD4+/CD8+ ratios, and reduced IL-4 expression compared with SAMR1 mice. The findings reinforce the potential of RAPA to modulate aging-related processes, highlighting improvements in mitochondrial function and energy metabolism across strains with different aging processes. However, the immunosuppressive effects of RAPA remain evident, even at low doses administered intermittently, in an age- and strain-specific manner. These findings emphasize the therapeutic potential of RAPA while underscoring the need for customized dosing strategies to balance efficacy and safety. These data highlight mitochondrial metabolic improvements as the primary benefit of intermittent low-dose RAPA and suggest potential clinical relevance for conditions involving compromised mitochondrial energy metabolism.
Practical considerations and emerging approaches for the management of vasomotor and sexual symptoms in breast cancer patients on endocrine therapies.
Expert Rev Clin Pharmacol
Jessica Fuhrman, Jina Yun, Amy Indorf
Vasomotor symptoms (VMS) and decreased libido are common menopausal symptoms. Patients with breast cancer receiving endocrine therapy experience new or worsening menopausal symptoms. Pharmacologic therapy for VMS has been centered on selective serotonin reuptake inhibitors and serotonin norepinephrine reuptake inhibitors, gabapentin, and clonidine. These therapeutic options fall short in obtaining adequate symptom relief, illustrating a therapeutic gap in efficacious treatment modalities. There are no historical systemic treatment options for low libido.
Fenofibrate as a Modulator of the Renin-Angiotensin System in Su/Hx-Induced Pulmonary Arterial Hypertension.
Int J Mol Sci
Karla M Rada-Pascual, Alejandra M Zúniga-Muñoz, Yamnia Q Alvarez-Alvarez +11 more
We evaluated the effects of fenofibrate (FF) in a SU5416/hypoxia model of pulmonary arterial hypertension (PAH) with a specific focus on its influence on the renin-angiotensin system (RAS). We assessed right ventricular systolic pressure (RVSP), mean pulmonary artery pressure (mPAP), medial pulmonary artery wall thickening, right ventricular (RV) hypertrophy, systolic pulmonary artery pressure (SPAP), pulmonary artery effective elastance (PAEa), RV diastolic pressure (RVDP), RV developed pressure (RVDevP), right ventricular-pulmonary arterial coupling index (RVPAC), RV dp/dt max and dp/dt min. Levels of angiotensin II, angiotensin (1-7), angiotensin-converting enzyme 2 (ACE2), Bmpr2, Smad5 and nitrite (NO2-) and nitrate (NO3-) in the lung and RV were evaluated. The expression of AT1R, MAS receptors, and ACE2 in lung tissue was assessed. FF prevented the increase in RVSP, mPAP, RV hypertrophy, reduced pulmonary arterioles remodeling, and attenuated the rise in SPAP, mPAP, and PAEa. In the RV, it reduced RVDevP and prevented the decrease in dp/dt min, without affecting RVDP. RVPAC showed partial improvement. In lung tissue, FF decreased angiotensin II levels, the Ang II/Ang-(1-7) ratio, and reduced angiotensin II receptor type 1 (AT1R) expression, while preserving the receptor for the angiotensin-(1-7) (MAS) and ACE2. FF tended to restore Bmpr2/Smad5 expression. NO2- levels were preserved and tended to preserve (NO3-) levels. In the RV, Ang-(1-7) increased, ACE2 was preserved, and NO2- and NO3 levels were maintained. FF exerts protective effects in Su/Hx-induced PAH.
Initial and evolutionary profile of adverse responders to an intensive weight loss intervention: the RESOLVE Study.
J Sports Med Phys Fitness
Mélina Bailly, Laurie Isacco, Frédéric Dutheil +14 more
There is a need to better identify adverse responders to weight-loss interventions. The aim of this study was to: 1) identify potential predictive factors of adverse responders to weight loss; and 2) follow their long-term evolution.
The effect of consuming different dietary protein sources at breakfast upon self rated satiety, peptide YY, glucagon like peptide-1, and subsequent food intake in young and older adults.
Eur J Nutr
Anthony W Watson, Anna Brooks, Lucy Moore +2 more
Interest in plant-based protein in the UK is increasing due to health, environmental, and ethical considerations. Recent studies have explored how different protein sources impact satiety and related gut hormone responses, with evidence suggesting varied responses between animal-based and plant-based proteins. Skewed protein intake patterns, especially at breakfast, present an opportunity for improving dietary protein distribution in populations who may require increased protein intake but often face appetite reductions. This study determined the acute effect of consuming a plant-based, high protein drink containing 30 g of protein (HPDp); an animal-based, high protein breakfast containing 30 g of protein (HPBa); and a low-protein (10 g), high-carbohydrate breakfast (HCLPB) on satiety hormone responses, subjective appetite and subsequent energy intake in older and younger populations when consumed at breakfast. Eighteen heathy adults completed this within-subject, counterbalanced, cross-over study, (12 under 35 years of age and six over 65 years of age). Measurements for appetite were obtained at baseline, 30, 60, 90, 120, 150, 180, 210 and 240 min, and plasma, GLP-1 and PYY at baseline, 30, 60, 90, 120, 180 min post breakfast consumption. No difference in appetitive responses was found between the HPDp and the energy- and protein-matched HPBa, with both eliciting greater GLP-1 and PYY (both p < 0.004) responses compared with a high carbohydrate, low protein meal. Subjective appetite was also suppressed to a greater extent with HPDp compared with HCLPB (p = 0.001). No differences were observed in ad libitum energy intake.
The Influence of Different Light Spectra on Broiler Chicken Endocrine Systems and Productivity.
Animals (Basel)
Lenuța Galan, Gheorghe Solcan, Carmen Solcan
In birds, light can penetrate the cranial bones and reach deep brain regions, where non-visual photoreceptors, especially in the hypothalamus, detect spectral and photoperiodic cues. Alongside retinal photoreception, deep-brain light sensing contributes to circadian entrainment and regulates melatonin secretion by the pineal gland. These light-driven pathways modulate endocrine activity, playing a key role in muscle development. This review explores how monochromatic light-emitting diode (LED) illumination, particularly green and blue wavelengths, affects the somatotropic axis (growth hormone-releasing hormone [GHRH]-growth hormone [GH]-insulin-like growth factor 1 [IGF-1]), the gonadal axis (gonadotropin-releasing hormone [GnRH]-luteinizing hormone [LH]/follicle-stimulating hormone [FSH]-sex steroids [testosterone, estrogen, progesterone]), the thyroid axis (thyrotropin-releasing hormone [TRH]-thyroid-stimulating hormone [TSH]-thyroxine [T4]/triiodothyronine [T3]), and the hypothalamic-pituitary-adrenal (HPA) axis (corticotropin-releasing hormone [CRH]-adrenocorticotropic hormone [ACTH]-corticosterone). Green light enhances early-stage muscle growth via GHRH and IGF-1 upregulation, while blue light supports later myogenic activity and oxidative balance. Light schedules also influence melatonin dynamics, which in turn modulate endocrine axis responsiveness to photic cues. Furthermore, variations in photoperiod and exposure to artificial lights at night (ALAN) affect thyroid activity and HPA axis reactivity, influencing metabolism, thermoregulation, and stress resilience. Together, ocular and intracranial photoreception form a complex network that links environmental light to hormonal regulation and muscle growth. These insights support the strategic use of LED lighting to optimize broiler performance and welfare.
Exploring the Role of Tripeptides in Wound Healing and Skin Regeneration: A Comprehensive Review.
Int J Med Sci
Siti Balqis Adnan, Manira Maarof, Mh Busra Fauzi +1 more
Wound healing is a complex and dynamic process that requires the coordination of cellular, molecular, and physiological events to restore tissue integrity. Despite notable advances in treatment strategies, optimizing healing outcomes, particularly in chronic wounds, remains a major challenge. Emerging evidence highlights the therapeutic promise of peptides, especially tripeptides, in accelerating tissue repair through diverse mechanisms. These short peptides regulate key processes such as cell migration, proliferation, and differentiation, while also modulating inflammation, promoting angiogenesis, and facilitating extracellular matrix (ECM) remodeling. This review, covering studies published between 2016 and 2025, explores the role of tripeptides in enhancing wound repair, emphasizing their biological functions, mechanisms of action, and therapeutic applications. Recent findings demonstrate that tripeptides can stimulate fibroblast migration, enhance collagen deposition, and support angiogenesis. In addition, they exhibit antimicrobial and anti-inflammatory properties, making them valuable candidates for both acute and chronic wound management. GHK-based formulations, including nanoparticle conjugates, hydrogels, and clinical derivatives such as TriHex and TriHex 2.0, enhance fibroblast migration, ECM remodeling, collagen and elastin synthesis, and wound closure while providing antimicrobial activity. KdPT mitigates hyperglycemia-induced oxidative stress and restores keratinocyte function, whereas KPV-loaded hydrogels reduce inflammation, promote tissue regeneration, and combat MRSA infections. Additionally, lipotripeptides (DICAMs) inhibit and disrupt bacterial biofilms, and GPE supports neuroprotection and regeneration through ERK and PI3K/Akt signaling activation. Beyond wound repair, this review also discusses comparative physicochemical properties and wound healing applications of tripeptides versus larger peptides, factors influencing their performance, strategies for combination with biomaterial scaffolds, and emerging applications in fields such as cancer and cosmetics. Collectively, tripeptides represent a promising class of multifunctional bioactive molecules in wound care, offering novel avenues for targeted tissue regeneration. Future research should focus on improving their stability, bioavailability, and delivery systems to fully harness their clinical potential in regenerative medicine.
Perceived benefits of treatment for obesity with retatrutide: A qualitative study of patients in a phase 2 clinical trial.
Obes Pillars
Iris A Goetz, Chisom Kanu, Anastasia Hoover +5 more
Retatrutide, an agonist of glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1, and glucagon receptors, is in development for the treatment of obesity. We interviewed participants exiting a phase 2 trial to understand the impact of retatrutide on eating behaviors, physical aspects, emotions, and lifestyle.
Dapagliflozin monotherapy and combination therapy with telmisartan ameliorate pregabalin-induced heart failure in rats.
Eur J Pharmacol
Zeinab M Awwad, Shimaa A Mahmoud, Shaimaa M Kh Abdelaziz +1 more
Heart failure (HF) associated with pregabalin (PRG) administration hampers its use in epilepsy, neuropathy and anxiety. Overactivation of cardiac renin angiotensin system (RAS) contributes to PRG-induced HF. The goal of the current study was to investigate the possible cardioprotective effects of dapagliflozin (DAPA), a selective sodium-glucose cotransporter 2 (SGLT2) inhibitor, compared with that of the combination therapy of DAPA and telmisartan (Tel) in attenuating PRG-associated HF by examining echocardiographic, morphometric and histopathological parameters. Moreover, to explore the possible beneficial impacts of DAPA and the combination therapy in guarding against PRG-induced myocardial alterations of angiotensin II (Ang II) and angiotensin 1-7 (Ang 1-7) levels, in addition to angiotensin converting enzyme (ACE), angiotensin converting enzyme 2 (ACE2), angiotensin II type 1 (AT1) receptor and Mas receptor (MAS1) levels. Results demonstrated that PRG use lead to echocardiographic, morphometric and histopathological detrimental changes and profoundly elevated ACE, Ang II and AT1 cardiac levels, while reduced cardiac ACE2, Ang 1-7 and MAS1 levels. Concurrent administration of either DAPA monotherapy or the combination therapy counteracted the deleterious echocardiographic, morphometric and histopathological alterations associated with PRG administration and showed notable protection against PRG-associated HF through activation of ACE2/Ang 1-7/MAS1 axis and suppression of ACE/Ang II/AT1 axis. However, the combination therapy group showed more cardioprotective effects than that of DAPA-treated group. The current findings provided the first evidence for the potential protective effects of DAPA monotherapy and combination therapy with Tel against PRG-induced altered balance between the two RAS axes.
Functional characterization and cAMP-mediated rescue of a novel truncating AVPR2 mutation causing nephrogenic diabetes insipidus.
Am J Physiol Endocrinol Metab
Diogo Manoel, Idris Mohammed, Khalid Hussain +1 more
Vasopressin plays a central endocrine role in water homeostasis by activating the arginine vasopressin receptor 2 (AVPR2) receptor in renal collecting duct cells. Mutations in AVPR2 are a leading cause of X-linked nephrogenic diabetes insipidus (NDI), a disorder marked by renal insensitivity to vasopressin, leading to polyuria, polydipsia, and hypernatremia. We identified a novel truncating AVPR2 mutation (c.570dup; D191*) in a pediatric patient with NDI and investigated its molecular and functional consequences using a renal epithelial cell model. The D191* mutant exhibited marked reduction in total and surface receptor expression due to intracellular retention and rapid proteasomal degradation. Functional assays revealed that 1-deamino-8-d-arginine vasopressin (dDAVP) stimulation failed to elicit cAMP production or activate downstream signaling targets, including CREB and ERK1/2, in cells expressing the mutant receptor. Aquaporin-2 (AQP2) membrane translocation, essential for water reabsorption, was also impaired. Notably, treatment with forskolin or 8-bromo-cAMP restored cAMP levels, reactivated downstream signaling, and rescued AQP2 localization to the apical membrane, independent of AVPR2 activation. These findings uncover the pathophysiological mechanism by which D191* impairs vasopressin signaling and suggest that bypassing the receptor via direct cAMP pathway activation offers a promising therapeutic strategy for NDI. This study highlights the endocrine relevance of precision molecular diagnostics and supports functional rescue approaches for receptor-based disorders.NEW & NOTEWORTHY This study identifies and functionally characterizes a previously unreported truncating AVPR2 mutation (c.570dup; p.D191*) causing congenital nephrogenic diabetes insipidus. Using renal epithelial cell models, the authors show that D191* leads to receptor misfolding, proteasomal degradation, absent cAMP signaling, and failure of aquaporin-2 trafficking. Remarkably, forskolin and 8-bromo-cAMP bypass the defective receptor to restore downstream signaling and water channel localization, highlighting a potential therapeutic strategy of receptor-independent cAMP activation for AVPR2-null nephrogenic diabetes insipidus.
Hyperosmolar hyperglycemic state with severe hypernatremia coexisting with central diabetes insipidus: A case report and literature review.
Open Life Sci
Congcong Yao, Lishuang Zhu, Songtao Shou +2 more
Diabetes insipidus is characterized by polyuria and polydipsia, often resulting from central or nephrogenic causes. In diabetic emergencies, hyperosmolar hyperglycemic state (HHS), severe hypernatremia, and ventricular fibrillation are life-threatening conditions that require prompt intervention. This report describes a 47-year-old male with poorly controlled diabetes mellitus, who developed coma, excessive thirst, polyuria, hyperglycemia (47.29 mmol/L), hypernatremia (195.6 mmol/L), and plasma hyperosmolality (385 mOsm/kg). Despite fluid resuscitation and insulin therapy, refractory hypernatremia persisted, leading to a diagnosis of central diabetes insipidus (CDI). The patient also developed ventricular fibrillation, which was managed with defibrillation. Concurrently, desmopressin and blood purification were administered to address CDI and severe hypernatremia. This case emphasizes the importance of considering CDI when polyuria persists despite glucose control. The occurrence of ventricular fibrillation underscores the necessity of continuous cardiac monitoring in the context of hypovolemia and severe electrolyte imbalance. We propose that diabetes mellitus-related vascular injury impairs blood flow in the hypothalamus-pituitary tract, disrupting arginine vasopressin synthesis and secretion, contributing to CDI in poorly controlled diabetes mellitus.
[Progress on tirzepatide, a GIP/GLP-1 receptor agonist, for the treatment of obesity-related obstructive sleep apnea].
Zhonghua Jie He He Hu Xi Za Zhi
L X Wang, Y Xiao
Obstructive sleep apnea (OSA) is a common sleep-disordered breathing. Obesity is one of the primary risk factors for OSA, while OSA itself may promote weight gain by impairing metabolism and increasing insulin resistance, thereby creating a vicious cycle. Together, these conditions pose a persistent public health challenge. In recent years, tirzepatide, a dual glucose-dependent insulinotropic polypeptide/glucagon-like peptide 1 (GIP/GLP-1) receptor agonist, has demonstrated therapeutic potential beyond weight loss in the management of obesity, encompassing various mechanisms. The recent SURMOUNT-OSA study showed that tirzepatide significantly reduced the apnea hypopnea index (AHI) in OSA patients and improved oxygen desaturation, blood pressure, and cardiovascular disease (CVD)-related risk factors. These effects are thought to be mediated not only by weight reduction, but also by modulation of fat distribution, inflammatory status, and autonomic nervous system function. This highlights the potential advantages of tirzepatide in obese patients with OSA. This review summarizes recent advances in tirzepatide research in this population, exploring its mechanisms of action, efficacy, and safety, with the aim of providing a theoretical basis for precision treatment strategies for OSA.
Carnosine protects against cerebral ischemia/reperfusion injury through promoting microglial M2 polarization via SIRT1/NF-κB signaling pathway.
Eur J Pharmacol
Ruili Ran, Yutong Wang, Ying Liu +4 more
Ischemic stroke, a leading cause of disability and mortality worldwide, often results in secondary brain injury due to oxidative stress and neuroinflammation following thrombolysis with tissue plasminogen activator (t-PA). Carnosine (CAR), a naturally occurring dipeptide, exhibits anti-inflammatory and neuroprotective properties. But its mechanisms in cerebral ischemia-reperfusion injury (CIRI) remain unclear. In this study, we aim to investigate the role of microglial polarization regulated by SIRT1/NF-κB signaling pathway on CAR therapeutic effect in CIRI. Here, we demonstrate that CAR attenuates neurological deficits and infarct volume in MCAO/R rats while promoting microglial polarization toward the anti-inflammatory M2 phenotype in vitro and in vivo. Mechanistically, CAR activates SIRT1, suppresses NF-κB signaling and downregulates pro-inflammatory cytokines (TNF-α, IL-1β). These effects were reversed by the SIRT1 inhibitor EX527, confirming the pivotal role of the SIRT1/NF-κB pathway. Therefore, our findings highlight CAR's potential as a therapeutic agent for ischemic stroke.
In Situ Monitoring of Phospholipid Flip-Flop via Fluorescence Self-quenching.
Chem Pharm Bull (Tokyo)
Hiroyuki Nakao, Yu Maeshiro, Keisuke Ikeda +1 more
Many antimicrobial peptides (AMPs) exert their activity by disrupting the integrity of the bacterial plasma membrane. One of the membrane-disrupting mechanisms of AMPs involves the formation of toroidal pores, composed of α-helices and lipid headgroups. These pores enable the diffusion of lipid molecules to the opposite leaflet without exposing their headgroups to the hydrocarbon core. Consequently, an increase in lipid transbilayer diffusion (flip-flop) in the presence of AMPs is an important characteristic for AMP structure and function. However, real-time monitoring of the rapid flip-flop in the presence of transmembrane pores has not been achieved because of the permeation of membrane-impermeable reagents and/or the low time resolution of the conventional assays. Herein, we have developed a fluorescence quenching-based flip-flop assay. The flip-flop rates obtained by our method were consistent with those measured by the conventional dithionite reduction assay, confirming the reliability of our approach. The real-time monitoring of the flip-flop process in the presence of the AMP, magainin 2, using the self-quenching assay suggested that the disordered toroidal pores composed of 2 magainin molecules facilitate flip-flop. The newly developed assay will provide a better understanding of the interactions between AMPs and lipid bilayers.
The Proteomic Analysis of Intermittent Fasting Alone or with GLP-1RA in NAFLD Rats.
Diabetes Metab Syndr Obes
Yimin Shao, Shengya Xu, Yuanyuan Ma +4 more
Intermittent fasting (IF) and glucagon-like peptide-1 receptor agonists (GLP-1RA) offer effective therapeutic options for nonalcoholic fatty liver disease (NAFLD). This study aimed to examine the effects of alternate-day fasting (ADF) alone and with liraglutide, and to explore the mechanisms behind each treatment.
Growth hormone in disease and treatment (Review).
Med Int (Lond)
Saikat Fakir, Md Matiur Rahman Sarker, Madan Sigdel +1 more
Growth hormone (GH) is a peptide hormone produced by the anterior pituitary gland, which regulates growth and development. Abnormal levels of GH have been associated with a diverse variety of disorders affecting life quality and longevity; including dwarfism, acromegaly, gigantism and cancer. Based on the fact that growth hormone-releasing hormone (GHRH) and somatostatin exert opposing effects on the regulation of GH, GHRH antagonists (GHRHAnts) and synthetic somatostatin analogs (SSAs) have been developed to alleviate GH-related illness. The present study provides information on the multifaceted role of GH in human health and disease. Furthermore, it summarizes recent findings on the protective effects of GHRHAnts and FDA-approved SSAs, such as octreotide, lanreotide and pasireotide, in GH-related and endothelium-dependent dysfunctions. Based on the provided bibliography, an emerging body of evidence suggests that GH modulators may represent a promising therapeutic possibility towards blood brain barrier dysregulation, keratitis, direct and indirect lung injury, sepsis, and acute respiratory distress syndrome.
Tβ4-17 peptide enhances the chemo-sensitivity of ovarian cancer cells to DDP by affecting NF-κB signaling pathway.
Med Oncol
Ling Guo, Haibing Wang, Nana Li +6 more
Ovarian cancer is a gynecologic malignancy with high mortality and poor prognosis. Chemoresistance is a key cause of ovarian cancer recurrence and metastasis. It has been found that some bioactive peptides can inhibit the growth and metastasis of cancer cells and promote cell apoptosis, thus exerting anti-cancer effects. Tβ4-17 is a small polypeptide that we selected using ITRAQ technology, and its precursor protein is thymosin β4. This study mainly investigated its effect in combination with cisplatin (DDP) on the proliferation, migration and apoptosis of ovarian cancer resistant cells and related molecular mechanisms. Our results showed that Tβ4-17 peptide combined with DDP significantly inhibited the proliferation and migration of drug resistance cells in ovarian cancer, promoted apoptosis, and increased the chemo-sensitivity of ovarian cancer cells to DDP. In addition, qRT-PCR and Western blot showed that NF-κB was significantly highly expressed in DDP-resistant cells of ovarian cancer. After application of NF-κB inhibitors and activators, Western blot, CCK8, EDU fluorescence proliferation assay, and cell scratch assay showed that Tβ4-17 peptide down-regulated NF-κB p65 protein expression and inhibited cell proliferation and migration. In conclusion, our study demonstrates that Tβ4-17 peptide enhances the sensitivity of ovarian cancer cells to DDP by down-regulating NF-κB expression.