Ask about this productRelated genes to: PLGF protein
- Gene:
- PGF NIH gene
- Name:
- placental growth factor
- Previous symbol:
- PGFL
- Synonyms:
- PLGF, PlGF-2, PlGF, SHGC-10760, D12S1900, PIGF
- Chromosome:
- 14q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-14
- Date modifiied:
- 2016-05-20
Related products to: PLGF protein
Related articles to: PLGF protein
- Huoxiang Zhengqi oral liquid (HXZQ), a classical herbal formulation used for gastrointestinal disorders, contains multiple bioactive constituents whose in vivo disposition remains incompletely understood. This study examined the role of gut microbiota in the biotransformation and pharmacokinetics of representative HXZQ constituents using integrated in vitro and in vivo approaches. Anaerobic incubation with gut microbiota was first used to assess metabolic susceptibility. A validated high-performance liquid chromatography-tandem quadrupole mass spectrometry (HPLC-QQQ-MS/MS) method was then developed for simultaneous quantification of 12 representative constituents. Pharmacokinetic profiles were subsequently compared in portal and systemic plasma after oral administration of HXZQ to normal and pseudo-germ-free (PGF) rats. The constituents exhibited heterogeneous microbiota-dependent metabolism. Flavonoid glycosides and triterpenoid saponins, including liquiritin apioside, liquiritin, glycyrrhizic acid, hesperidin, and narirutin, underwent extensive microbial transformation, with transient formation of corresponding aglycones. In contrast, lignans and coumarins showed limited conversion. Pharmacokinetic analysis showed that gut microbiota significantly influenced portal and systemic exposure of several constituents. In PGF rats, exposure to key aglycones, including 18-β-glycyrrhetinic acid, isoliquiritigenin, and liquiritigenin, was markedly reduced, whereas exposure to parent glycosides, such as glycyrrhizic acid, increased. Some compounds were detected in portal plasma but not systemic plasma, indicating limited systemic availability. Moreover, magnolol and byakangelicin exposure was significantly decreased in PGF rats despite weak direct microbial susceptibility in vitro. These findings indicate that HXZQ pharmacokinetics is strongly shaped by microbiota-dependent metabolism and post-absorption disposition, providing insight into host-microbiota-herb interactions. - Source: PubMed
Publication date: 2026/09/06
Wang LinweiWang YangyangXu ZhouTian XiaotingHuang ChenggangGuo XiaozhenZhao Yongshan - Developing low-cost, efficient, and durable electrocatalysts for CO conversion remains a significant challenge. Herein, we report a Co-metalated porphyrinic pillared graphene framework (Co-P-PGF) that functions as a single-atom catalyst (SAC) for efficient electrochemical CO reduction. The framework was synthesized via Sonogashira-Hagihara coupling between Co-porphyrin linkers and iodobenzene-functionalized reduced graphene oxide (rGO), alongside a metal-free analogue (P-PGF). The atomically dispersed Co(II) centers serve as active sites for CO binding and activation, while the conductive rGO sheets facilitate rapid electron transport and efficient charge transfer at the electrode-electrolyte interface. Owing to the integrated conductive graphene architecture, Co-P-PGF exhibits excellent intrinsic electrocatalytic activity without requiring additional conductive carbon additives. The catalyst achieves a remarkable Faradaic efficiency for CO production (FE = 94.07%) in aqueous electrolyte in an H-cell configuration. Furthermore, operation in a flow cell results in a six-fold enhancement in current density compared to the H-cell. Operando DRIFTS, Raman spectroscopy, and X-ray absorption spectroscopy, complemented by density functional theory calculations, reveal the nature of the active sites and reaction intermediates during CO reduction. These results highlight the promise of graphene-based SACs as cost-effective, sustainable, and high-performance catalysts for electrochemical CO reduction reaction (CORR). - Source: PubMed
Publication date: 2026/09/10
Rahimi Faruk AhamedBarman SoumitraMandal TamagnaJena RohanDey AnupamGhosh AdrijaSamanta DebabrataDahiya RituKumar RaviMaji SouravMakineni Surendra KumarBhattacharyya DibyenduMaji Tapas Kumar - γ-Linolenic acid (GLA) is an n-6 polyunsaturated fatty acid (PUFA) with reported vasoprotective effects. GLA has been shown to inhibit contractions in pig coronary arteries via competitive antagonism at prostanoid TP receptors. α-Linolenic acid (ALA), an n-3 PUFA and a structural isomer of GLA, has been shown to inhibit contractions in pig basilar arteries (PBAs) via prostanoid TP receptor antagonism and activation of K channels. However, the actions of GLA in cerebral arteries remain unclear. In this study, we examined the effects of GLA on contractile responses in PBAs. GLA (10-10 M) concentration-dependently inhibited contractions induced by the TP receptor agonist U46619 (3 × 10 M) and prostaglandin F (PGF; 3 × 10 M). GLA (3 × 10-3 × 10 M) shifted the concentration-response curve for U46619 to the right. Schild analysis yielded a slope of 1.33 (95% confidence interval: 0.70-1.96), which was not significantly different from unity, but GLA also reduced the maximal response to U46619. The apparent pA value was 5.43. GLA (10 M) also inhibited PGF-induced contractions in the presence of the TP receptor antagonist SQ 29,548 (10 M); this inhibitory effect was attenuated by Ba (10 M) but not by other tested K channel inhibitors. GLA also inhibited endothelin-1 (10-3 × 10 M)-induced contractions, and this effect was attenuated by Ba. These findings indicate that GLA, like ALA, suppresses contractile responses in PBAs through dual mechanisms involving TP receptor antagonism and activation of Ba-sensitive K channels. - Source: PubMed
Yoshioka KentoInagaki MinamiPhi Tam MinhKimura HarukiOsa KeigoObara KeisukeNakamichi NoritakaTanaka Yoshio - Polychlorinated biphenyls (PCBs) are persistent organic pollutants of global concern, yet their associations with predicted cardiovascular risk remain unclear. In this prospective Wuhan-Zhuhai cohort study, concentrations of seven serum PCBs (PCB-28, 52, 101, 118, 138, 153, and 180) were measured using GC-MS/MS. The validated China-PAR equation was used to calculate predicted 10-year atherosclerotic cardiovascular disease (ASCVD) risk, and urinary 8-iso-prostaglandin F2α (8-iso-PGF) served as a marker of oxidative stress. Multivariable linear and logistic regression models were fitted to evaluate PCB-related differences in continuous predicted risk and predicted high-risk status. Cross-sectionally, each one-unit increase in ln-transformed PCB-118, PCB-138, PCB-153, and ΣPCB was associated with 1.249-, 1.253-, 1.457-, and 1.829-percentage-point higher predicted 10-year ASCVD risk, respectively (all P < 0.05). The associations for PCB-118, PCB-138, and PCB-153 remained significant after FDR correction. Longitudinally, persistent high PCB-118 exposure was associated with a 0.510 percentage-point greater increase in predicted 10-year ASCVD risk (95 % confidence interval [CI]: 0.023-0.996, P < 0.05) and a higher risk of transitioning to predicted high-risk status (RR = 1.432, 95 % CI: 1.012-2.027, P < 0.05) compared with persistent low exposure, although neither association remained significant after FDR correction. Exploratory mediation analysis suggested that urinary 8-iso-PGF was statistically consistent with partial indirect pathways for the associations, with estimated indirect proportions ranging from 3.29 % to 11.62 %. Database-derived bioinformatics analyses highlighted TNF/NF-κB/IL-17 pathways and identified IL-6, TNF, IL-1β, and ICAM1 as candidate hub genes. Overall, several PCB measures were cross-sectionally associated with higher predicted ASCVD risk, whereas longitudinal evidence was limited and was strongest for persistent high PCB-118 exposure. Exploratory mediation and bioinformatics findings highlighted possible oxidative-stress and inflammation-related pathways that require further validation. - Source: PubMed
Publication date: 2026/08/30
Yao YuxinChen BingdongDai JianghongLiang RuyiZhang JiakeWang MengyiTan QiyouDing XuejieGuo YanjunWang DongmingWang BinYin HaoyuShang BingxinYou XiaojieMa JixuanZhou MinChen Weihong - Atypical superimposed preeclampsia (sPE) developing before 20 weeks of gestation is extremely rare, and its pathophysiology remains unclear. We herein report three women with underlying chronic hypertension or IgA nephropathy who developed severe hypertension, worsening proteinuria, and fetal growth restriction or fetal death before 20 weeks of gestation. All cases showed markedly elevated soluble fms-like tyrosine kinase-1/placental growth factor (sFlt-1/PlGF) ratios (617-1357), and placental pathology demonstrated maternal vascular malperfusion. Maternal clinical manifestations promptly improved after the termination of pregnancy. All three women subsequently achieved successful pregnancies with appropriate management. These results suggest that atypical sPE shares the angiogenic imbalance and placental pathology characteristic of conventional preeclampsia. Although limited by the small number of cases, these results provide additional insights into the pathophysiology of atypical sPE and suggest a role for angiogenic biomarkers in evaluating placental dysfunction. - Source: PubMed
Ito ChisaOgoyama ManabuOhkuchi AkihideSuzuki HirotadaTakahashi HironoriFujiwara Hiroyuki