Search Results (489)

Bassia scoparia (Syn. Kochia scoparia (L.) Schrad.) is a medicinal plant whose fruit, Kochiae Fructus, has been extensively studied for its dermatological applications. This study focused on extracts from the whole plant B. scoparia (WPBS), excluding fruits, to address the research gap regarding the medicinal properties of non-fruit parts. The diverse skin benefits of WPBS, including its anti-photoaging, moisturizing, wound healing, anti-inflammatory, and anti-angiogenic effects, were investigated. The WPBS extract enhanced the viability of keratinocytes (HaCaT) without inducing cytotoxic effects. WPBS significantly reduced matrix metalloproteinase-1 (MMP-1) levels and increased collagen type I alpha 1 (COL1A1) levels (p < 0.01) in fibroblasts exposed to ultraviolet B (UVB) radiation, indicating strong anti-photoaging effects. WPBS upregulated skin hydration markers such as aquaporin-3 (AQP3) and hyaluronan synthase-3 (HAS3) and effectively accelerated fibroblast wound closure compared to the positive control. Furthermore, WPBS substantially downregulated the expression of inflammatory (COX-2 and IL-1β) and angiogenic markers (VEGF). Transcriptome analysis (RNA-seq) confirmed that WPBS suppressed inflammation-related and UV-induced gene expression pathways. Overall, these findings expand the therapeutic scope of B. scoparia beyond its traditional fruit use and suggest that WPBS is a promising botanical ingredient for various skin applications. Full article

Objective: To investigate the effects of oat fiber on animal constipation and elucidate its underlying mechanisms. Methods: Male BALB/c mice were randomly allocated into five groups: control group (CON), model control group (MODEL), low dose group (LOW), middle dose group (MIDDLE), high dose group (HIGH). Constipation was induced in the mice by intragastric administration of loperamide. Subsequently, the mice (except those in the CON and MODEL groups) were administered oat fiber intragastrically for 21 consecutive days. Results: Compared with the MODEL group, oat fiber significantly increased the number of fecal pellets, fecal wet weight, and fecal water content (p < 0.05), shortened the time to first black stool excretion (p < 0.05), and enhanced the small intestinal propulsion rate in constipated mice. Additionally, oat fiber significantly upregulated motilin (MTL) and gastrin (GAS) levels (p < 0.05), while downregulating vasoactive intestinal peptide (VIP) and somatostatin (SS) levels (p < 0.05). It also significantly reduced the transcription level of Aquaporin 8 (AQP8) (p < 0.05), effectively alleviating intestinal mucosal injury and immune inflammation. The relative expression levels of TNF-α and IL-1β were significantly decreased in the oat fiber group (p < 0.05). Gut microbiota analysis revealed that oat fiber increased both the abundance and diversity of gut microbiota in constipated mice. Specifically, oat fiber was found to enhance the relative abundance of Firmicutes while reducing that of Bacteroidetes. At the genus level, it promoted the proliferation of Lachnospiraceae_NK4A136_group and Roseburia. Conclusions: Oat fiber alleviates constipation in mice by modulating gastrointestinal regulatory peptides, gut microbiota, aquaporin and mitigating intestinal barrier damage and immune-inflammatory responses. Full article

Dendrobium, a prominent genus in the Orchidaceae family, has generated significant research attention due to its demonstrated biological potential, particularly its notable anti-inflammatory and antioxidant activities. In this study, two fractions of fermented Dendrobium officinale polysaccharides (FDOPs) were successfully isolated through a multi-stage purification strategy including gradient ethanol precipitation, gel column chromatography, and ion exchange chromatography with Lactobacillus reuteri CCFM863. Structural characterization revealed that both Dendrobium officinale polysaccharide fractions consisted of (1→4)-β-D-Manp, (1→4)-β-D-Glcp, and (1→4)-α-D-Glcp residues. The anti-inflammatory efficacy and keratinocyte-protective potential of FDOPs (FDOP-1A and FDOP-2A) were investigated by using lipopolysaccharide (LPS)-induced RAW264.7 and HaCaT cells models, which showed significant inhibitions on the inflammatory factors of monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), nitric oxide (NO), and interleukin-1 beta (IL-1β); recovered levels of filaggrin (FLG), aquaporin 3 (AQP3), transient receptor potential vanilloid 4 (TRPV4), cathelicidin antimicrobial peptide (CAMP)/LL-37, and adiponectin (ADIPOQ); and the reduced protein expression of the TLR4/IκB-α/NF-κB/NLRP3 pathway. Notably, the FDOPs exhibited a remarkable reactive oxygen species (ROS) scavenging capacity, demonstrating superior antioxidant activity. Therefore, FDOPs show dual anti-inflammatory and antioxidant properties, making them suitable as active ingredients for modulating epidermal inflammation and promoting skin barrier repair. Full article

Introduction: This study aims to elucidate the impact of AQP1 on cardiac function and the intestinal microbiota in mice with chronic heart failure and to further investigate the broad effects of AQP1 on the gut microbiota composition in these mice. Methods: AQP1 knockout mice were used as the experimental group, with wild-type mice serving as the control group. The study evaluated the effects of AQP1 on various physiological parameters, including blood pressure, heart rate, cardiac function, cardiac color Doppler ultrasound, and 24 h urine collection. Additionally, the high-throughput sequencing of gut microbiota was performed to identify key microbial communities. Results: The deletion of the AQP1 gene did not significantly alter key cardiovascular metrics such as systolic blood pressure (SBP), mean blood pressure (MBP), or left ventricular mass (LV mass). However, we found that AQP1 knockout affected 24 h urine output in mice. Echocardiography results showed that AQP1 expression influenced LV mass, LVAW; d, and LVPW; s. Moreover, substantial differences were observed in the intestinal microbiota profiles between AQP1 knockout mice with heart failure and their wild-type counterparts. These findings suggest that AQP1 may contribute to cardiac dysfunction in mice with chronic heart failure through the regulation of gut microbiota. Conclusion: Our investigation provides initial insights into the role of AQP1 in modulating the intestinal microbiota in a murine model of heart failure. However, the precise mechanisms underlying this association require further exploration and detailed analysis. Full article

Aquaporins in rice (Oryza sativa L.) represent a pivotal class of transmembrane channel proteins that mediate the bidirectional transport of water and small solutes, which have critical functions in cellular osmoregulation and ion homeostasis maintenance. Their evolutionary diversity and functional plasticity constitute fundamental mechanisms underlying the adaptive responses to diversified environmental challenges. This review systematically summarizes rice AQPs’ evolutionary origins, structural characteristics, and spatiotemporal expression patterns under both physiological and stress conditions, highlighting the high conservation of their key functional domains across evolution and their environment-driven functional diversification. The molecular mechanisms governing AQPs in water utilization, nutrient uptake, and stress responses are unraveled. Furthermore, the potential of precision gene editing and multi-omics integration is discussed to decipher the intricate relationships between AQP evolutionary history, environmental adaptability, and functional specialization, thereby providing a theoretical basis for advancing crop stress resistance and high-quality breeding. Full article

Proton therapy is increasingly used to treat pediatric and adult brain tumors, but there is still uncertainty surrounding the biological effects of protons on the heart. Also, the molecular and functional responses to proton irradiation are still unknown. This study investigates the effect of protons on cardiac disease by comparing their effects on the hearts of rats exposed to hypergravity. A total of 20 Sprague Dawley rats were tested, including a group that was irradiated with 0.1 Gy of protons to the heart, a group exposed to hypergravity, a group exposed to both protons and hypergravity, and a control group. Changes in AQP4, calcium homeostasis, and fibrosis-related markers were investigated using Western blotting, immunohistochemistry, etc. The proton-irradiated group showed no changes compared to the control group. In rats exposed to hypergravity, the cardiac fibrosis markers TGF-ꞵ1, MMP9, and MMP2 were increased. On the other hand, the group exposed to hypergravity followed by proton irradiation tended to display a significant decrease in these markers. Along with reduced fibrosis-related markers, the consistent tendency was also confirmed in the cardiac calcium homeostasis-related proteins and AQP4 through Western blotting. In summary, our findings indicate that rats subjected to hypergravity experienced both cardiac hypertrophy and fibrosis, while proton therapy appeared to mitigate the effects of cardiac disease. These results suggest that proton therapy prevents heart disease triggered by hypergravity, providing insights for protecting astronauts’ cardiovascular health. Full article

Alcoholic liver disease (ALD) is a type of liver disease with complex pathogenic factors. In 2019, alcohol caused 11 million life-years to be lost globally, and the mortality rate has continued to rise. This study aims to explore the exclusive gene profile of AH and construct an mRNA-lncRNA regulatory network through an integrative analysis and database validation to reveal potential key biomarkers. We obtained expression data for alcoholic hepatitis from the GEO database; screened differentially expressed genes (DEGs) through a weighted gene co-expression network analysis (WGCNA); conducted a GO&KEGG analysis; and focused on the enrichment pathways for the top 20 genes. Hub genes were selected using cytoHubba and MCODE to construct the mRNA-lncRNA regulatory network, and key genes were confirmed using GSE167308 and GSE28619. We obtained 2552 differentially expressed mRNAs and 555 differentially expressed lncRNAs from three databases. Differentially expressed genes are mainly involved in pathways such as lipid metabolism disorders, complement activation, the activation of cancer-related pathways, the excessive activation of inflammatory immunity, and the initiation of cell adhesion and fibrosis. Based on the hub gene analysis, we screened out 43 key genes. By constructing the key mRNA-lncRNA–pathway network, we identified 12 mRNAs (AQP1, ELOVL7, ITPR3, KRT19, KRT23, LAMC2, MMP7, PROM1, SPINT1, STK39, TNFRSF21, and VTCN1) and 14 lncRNAs that play an important role in the occurrence and development of alcoholic hepatitis. To sum up, this article mainly expounds upon the key genes in the occurrence and development of alcoholic hepatitis. The key genes are mainly concentrated within signaling pathways such as metabolic pathways, fatty acid metabolism, and cancer pathways. Twelve differentially expressed mRNAs in the co-expression network can be used as biomarkers and intervention targets for the diagnosis and treatment of alcoholic hepatitis. Full article

Background/Objectives: Cellular oxidative stress is crucial for GV stage oocyte vitrification quality. PI3K and the aquaporin family have been shown to facilitate various cellular processes related to redox homeostasis and energy balance; yet, the mechanisms underlying the involvement of aquaporin 7 (AQP7) in vitrified oocyte oxidative stress remain unclear. The purpose of the present investigation was to evaluate the role of AQP7 in vitrified oocytes and the mechanisms involved. Methods: AQP7 inhibitors were employed to investigate the effect of AQP7 on oxidative stress in mouse-vitrified oocytes, whereas PI3K activators were harnessed to ascertain whether AQP7 serves as a functional molecule involved in this process. Results: Our results indicate that AQP7 inhibition in vitrified oocytes results in a significant decrease in glutathione (GSH) levels associated with cellular oxidation and an elevation in H₂O₂ levels. This was accompanied by exacerbated mitochondrial dysfunction, weakened cytoskeletal proteins, accelerated early apoptosis. Consequently, both survival and maturation rates were markedly reduced. Interestingly, PI3K/AKT activation increased AQP7 expression, restored abnormal mitochondrial distribution, as well as calcium homeostasis, and rescued the oocyte survival/maturation rate. Conclusions: Our results provide new insights indicating that PI3K/AKT/AQP7 decreases oxidative stress by regulating mitochondrial morphology, function, and distribution, thereby rescuing oocyte maturation in vitrification. Full article

Topmouth Gudgeon (Pseudorasbora parva), a typical invasive fish worldwide, has successfully invaded various aquatic ecosystems and colonized saline–alkali waters from freshwater due to its broad environmental tolerances. However, the molecular mechanisms of adaptation to saline–alkali stress for P. parva remain poorly characterized. To explore the potential genetic mechanisms, we conducted differential gene expression analysis using gill transcriptome of wild P. parva populations collected from four waters with different salinity–alkalinity levels. Comparative transcriptomics analysis showed that DEGs involved in osmoregulation, ano6, cftr, aqp1, and aqp3, were down-regulated; DEGs related to ammonia excretion, Rhcg and Rhbg, were up-regulated; DEGs for acid–base accommodation, nhe2, slc4a1, and ca2, were down-regulated while ca4 was up-regulated; and immune-system-related DEGs, il8 and il17, were down- and up-regulated, respectively, in a high saline–alkaline water environment. The DEGs were enriched in multiple KEGG pathways, such as the ribosome, thermogenesis, oxidative phosphorylation, necroptosis, and HIF-1 signaling pathways. In addition, more DEGs were significantly enriched in immune-disease-related pathways in high saline–alkaline water populations. This suggests that P. parva exposed to chronic saline–alkali stress, despite survival, still needed immune system regulation to defend against potential diseases. These results revealed the gill molecular mechanisms underlying P. parva saline–alkaline adaptation and offered valuable insights into the development of saline–alkaline water aquaculture fisheries Full article

This study investigated the potential cosmetic properties of the ethyl acetate (EtOAc) fraction obtained from the roots of Astilboides tabularis (Hemsl.) Engl., focusing on skin-whitening, antiwrinkle, and moisturizing effects using cell-based assays and three-dimensional (3D) artificial skin models (Neoderm-ED and Neoderm-ME). The EtOAc fraction showed significant dose-dependent inhibitory activity against tyrosinase (TYR) (72.0% inhibition at 50 µg/mL), comparable to that of kojic acid. In α-melanocyte-stimulating hormone (α-MSH)-stimulated Neoderm-ME artificial skin containing melanocytes, the EtOAc fraction reduced melanin synthesis at concentrations of 50 and 75 µg/mL and decreased melanogenesis-related gene expression, including TYR, microphthalmia-associated transcription factor (MITF), tyrosinase-related protein-1 (TRP-1) and TRP-2. In the antiwrinkle assays, the EtOAc fraction effectively inhibited elastase activity (41.5% inhibition at 10 µg/mL), exceeding the efficacy of ursolic acid. In the Neoderm-ED artificial skin model, the EtOAc fraction reversed structural damage induced by particulate matter (PM10), restoring epidermal thickness and dermal density. This improvement was supported by the increased expression of skin barrier and antiwrinkle genes, including filaggrin, hyaluronic acid synthase-1 (HAS-1), HAS-2, aquaporin-3 (AQP-3), collagen type I alpha 1 chain (COL1A1), elastin, tissue inhibitor of metalloproteinases-1 (TIMP-1), and TIMP-2, as well as decreased expression of matrix metalloproteinases (MMP-1, MMP-3, and MMP-9). Our results indicate that the EtOAc fraction from A. tabularis root has considerable potential as a multifunctional cosmetic. Full article

This study investigated the effects of potassium magnesium sulfate (PMS) on intestinal dissociation and absorption rate, immune function, and expression of the NOD-like receptor thermal domain-associated protein 3 (NLRP3) inflammasome, aquaporins (AQPs), and potassium and magnesium ion channels in weaned piglets. Experiment 1 involved the assessment of the dissociation rate of PMS in pig digestive fluid and the absorption rate of PMS in the small intestine using an Ussing chamber in vitro. In Experiment 2, 216 healthy 21-day-old weaned piglets were selected and randomly assigned to six groups (0%, 0.15%, 0.30%, 0.45%, 0.60%, and 0.75% PMS), with each group 6 replicates of six piglets per replicate. The in vitro Ussing chamber results indicated that the absorption of K⁺ and Mg²⁺ in the jejunum and ileum was significantly higher than that in the duodenum (p < 0.05). The in vivo study demonstrated that the addition of PMS resulted in a linear increase in serum K⁺, IgG, and interleukin (IL)-2 levels while simultaneously reducing serum IL-1β levels (p < 0.05). Dietary PMS significantly elevated serum IL-10 and Mg²⁺ levels in feces (p < 0.05). Furthermore, supplementation with 0.60% or 0.75% PMS significantly downregulated the mRNA expression of NLRP3 in the jejunum (p < 0.05). Dietary PMS supplementation linearly reduced the mRNA expression levels of cysteine protease 1 (Caspase-1) and IL-1β in both the jejunum and colon as well as the mRNA expression levels of two-pore domain channel subfamily K member 5 (KCNK5) in these regions (p < 0.05). Notably, supplementation with 0.15% PMS significantly decreased the mRNA expression of transient receptor potential channel 6 (TRPM6) in the jejunum and significantly increased the expression of TRPM6 in the colon (p < 0.05). Dietary addition of 0.45% and 0.60% PMS significantly increased the mRNA expression of aquaporin 3 (AQP3) in the colon (p < 0.05), whereas 0.75% PMS significantly increased the mRNA expression of aquaporin 8 (AQP8) in both the jejunum and colon. Moreover, the expression levels of AQP3 and AQP8 were significantly negatively correlated with the diarrhea rate observed between days 29 and 42. In conclusion, dietary PMS supplementation improved immune function, inhibited the activation of intestinal NLRP3, and modulated the expression of water and ion channels in weaned piglets, thereby contributing to the maintenance of intestinal water and ion homeostasis, which could potentially alleviate post-weaning diarrhea in piglets. The recommended supplemental level of PMS in the corn-soybean basal diet for weaned piglets is 0.30%. Full article

Aquaporin 1 is a membrane water channel protein, which was studied here in spiny dogfish (Squalus acanthias) osmoregulatory tissues using a variety of techniques. The cloning of aquaporin 1 (AQP1) in the spiny dogfish identified a splice variant version of the mRNA/protein (AQP1SV1/AQP1SV1). Polymerase chain reaction (PCR) in a range of tissues showed AQP1 to be expressed at very high levels in the rectal gland with ubiquitous mRNA expression at lower levels in other tissues. Northern blotting showed that AQP1 had a mRNA size of 5.3 kb in kidney total RNA. The level of AQP1 mRNA was significantly lower in the rectal glands of fish acclimated to 120% seawater (SW; vs. 75% SW (p = 0.0007) and 100% SW (p = 0.0025)) but was significantly higher in those fish in the kidney (vs. 100% SW (p = 0.0178)) and intestine (vs. 75% SW (p= 0.0355) and 100% SW (p = 0.0285)). Quantitative PCR determined that AQP1SV1 mRNA levels were also significantly lower in the rectal glands of both 120% (p = 0.0134) and 100% SW (p = 0.0343) fish in comparison to 75% SW-acclimated dogfish. Functional expression in Xenopus oocytes showed that AQP1 exhibited significant apparent membrane water permeability (p = 0.000008–0.0158) across a range of pH values, whereas AQP1SV1 showed no similar permeability. Polyclonal antibodies produced against AQP1 (AQP1 and AQP1/2 antibodies) and AQP1SV1 had bands at the expected sizes of 28 kDa and 24 kDa, respectively, as well as some other banding. The weak AQP1 antibody and the stronger AQP1/2 antibody exhibited staining in the apical membranes of rectal gland secretory tubules, particularly towards the periphery of the gland. In the gill, the AQP1/2 antibody in particular showed staining in secondary-lamellar pavement-cell basal membranes, and in blood vessels and connective tissue in the gill arch. In the spiral valve intestine side wall and valve flap, the AQP1/2 antibody stained muscle tissue and blood vessel walls and, after tyramide signal amplification, showed some staining in the apical membranes of epithelial cells at the ends of the luminal surface of epithelial folds. In the rectum/colon, there was also some muscle and blood vessel staining, but the AQP1 and AQP1/2 antibodies both stained a layer of cells at the base of the surface epithelium. In the kidney convoluted bundle zone, all three antibodies stained bundle sheath membranes to variable extents, and the AQP1/2 antibody also showed staining in the straight bundle zone bundle sheath. In the kidney sinus zone, the AQP1/2 antibody stained the apical membranes of late distal tubule (LDT) nephron loop cells most strongly, with the strongest staining in the middle of the LDT loop and in patches towards the start of the LDT loop. There was also a somewhat less strong staining of segments of the first sinus zone nephron loop, particularly in the intermediate I (IS-I) tubule segment. Some tubules appeared to show no or only low levels of staining. The results suggest that AQP1 plays a role in rectal gland fluid secretion, kidney fluid reabsorption and gill pavement-cell volume regulation and probably a minor role in intestinal/rectal/colon fluid absorption. Full article

Peripheral blood leukocytes are able to migrate to the inflamed tissue, and to engulf and kill invading microbes. This requires rapid modifications of cell morphology and volume through fast movements of osmotic water into or out of the cell. In this process, membrane water channels, aquaporins (AQPs), are critical for cell shape changes as AQP-mediated water movement indirectly affects the cell cytoskeleton and, thereby, the signaling cascades. Recent studies have shown that the deletion or gating of two immune cell AQPs, AQP3 and AQP9, impairs inflammation and improves survival in microbial sepsis. Here, we assessed the expression and distribution of AQP3 and AQP9 in human leukocytes and investigated their involvement in the phagocytosis and killing of the Gram-negative pathogenic bacterium Klebsiella pneumoniae, and their role in lipopolysaccharide (LPS)-induced cell migration. By RT-qPCR, AQP3 mRNA was found in peripheral blood mononuclear cells (PBMCs) but it was undetectable in polymorphonuclear white blood cells (PMNs). AQP9 was found both in PBMCs and PMNs, particularly in neutrophil granulocytes. Immunofluorescence confirmed the AQP3 expression in monocytes and, to a lesser degree, in lymphocytes. AQP9 was expressed both in PBMCs and neutrophils. Specific inhibitors of AQP3 (DFP00173) and AQP9 (HTS13286 and RG100204) were used for bacterial phagocytosis and killing studies. No apparent involvement of individually blocked AQP3 or AQP9 was observed in the phagocytosis of K. pneumoniae by neutrophils or monocytes after 10, 30, or 60 min of bacterial infection. A significant impairment in the phagocytic capacity of monocytes but not neutrophils was observed only when both AQPs were inhibited simultaneously and when the infection lasted for 60 min. No impairment in bacterial clearance was found when AQP3 and AQP9 were individually or simultaneously blocked. PBMC migration was significantly impaired after exposure to the AQP9 blocker RG100204 in the presence or absence of LPS. The AQP3 inhibitor DFP00173 reduced PBMC migration only under LPS exposure. Neutrophil migration was considerably reduced in the presence of RG100204 regardless of whether there was an LPS challenge or not. Taken together, these results indicate critical but distinct involvements for AQP3 and AQP9 in leukocyte motility, while no roles are played in bacterial killing. Further studies are needed in order to understand the precise ways in which these two AQPs intervene during bacterial infections. Full article

Aquaporins (AQPs) are a family of transmembrane water channel proteins facilitating the transport of water and, in some cases, small solutes such as glycerol, lactate, and urea. In the central nervous system (CNS), several aquaporins play crucial roles in maintaining water homeostasis, modulating cerebrospinal fluid (CSF) circulation, regulating energy metabolism, and facilitating neuroprotection under pathological conditions. Among them, AQP2, AQP4, AQP9, and AQP11 have been implicated in traumatic and non-traumatic brain injuries. The most abundant aquaporin (AQP) in the brain, AQP4, is essential for fluid regulation, facilitating water transport across the blood–brain barrier and glymphatic clearance. AQP2 is primarily known for its function in the kidneys, but it is also expressed in brain regions related to vasopressin signaling and CSF dynamics. AQP9 acts as a channel for glycerol and lactate, thus playing a role in metabolic adaptation during brain injury. AQP11, an intracellular aquaporin, is involved in oxidative stress responses and cellular homeostasis, with emerging evidence suggesting its role in neuroprotection. Aquaporins play a dual role in brain injury; while they help maintain homeostasis, their dysregulation can exacerbate cerebral edema, metabolic dysfunction, and inflammation. In traumatic brain injury (TBI), aquaporins regulate the formation and resolution of cerebral edema. In non-traumatic brain injuries, including ischemic stroke, aneurysmal subarachnoid hemorrhage (aSAH), and intracerebral hemorrhage (ICH), aquaporins influence fluid balance, energy metabolism, and oxidative stress responses. Understanding the specific roles of AQP2, AQP4, AQP9, and AQP11 in these brain injuries may lead to new therapeutic strategies to mitigate secondary damage and improve neurological outcomes. This review explores the function of the above aquaporins in both traumatic and non-traumatic brain injuries, highlighting their potential and limitations as therapeutic targets for neuroprotection and recovery. Full article

Plant aquaporin proteins (AQPs) are categorized into seven distinct families, among which, plasma membrane intrinsic proteins (PIPs) play pivotal roles in plant growth and physiological processes. In this study, we identified 11 CpPIP genes in wintersweet (Chimonanthus praecox (L.) Link) based on bioinformatic characterization of gene structural organization, chromosomal localization, and phylogenetic relationships. Subsequent phylogenetic reconstruction resolved two evolutionarily distinct CpPIP subclasses. We focused on the isolation and characterization of CpPIP1;1, which showed the highest expression in floral organs. During flowering, a significant increase was observed in the expression of the CpPIP1;1 gene in response to a gradual reduction in environmental temperature. Moreover, the overexpression of CpPIP1;1 in Arabidopsis thaliana resulted in early flowering and an enhanced tolerance to salt, drought, and cold stress. We subsequently transcriptionally fused the CpPIP1;1 promoter containing MYC and MYB low-temperature response elements to the β-glucuronidase (GUS) reporter gene and introduced this construct into Nicotiana tabacum. GUS activity assays of the transgenic plants revealed that the CpPIP1;1 promoter was effectively expressed in flowers. Furthermore, the promoter transcriptional activity was enhanced in response to salt, drought, cold, gibberellic acid, and methyl jasmonate treatments. Collectively, our findings in this study revealed that CpPIP1;1 plays a key role in the regulation of flowering and stress tolerance in wintersweet plants. Full article