[Excretion of three alkaloids from Simiao Pills in urine, feces, and bile between normal and type 2 diabetic rats].

This study investigated the differences in excretion kinetics of three alkaloids and their four metabolites from Simiao Pills in normal and type 2 diabetic rats. The diabetes model was established in rats by injection of streptozotocin, and the alkaloids in urine, feces, and bile of normal and diabetic rats were detected by LC-MS/MS to explore the effect of diabetes on alkaloid excretion of Simiao Pills. The results showed that 72 h after intragastric administration of the extract of Simiao Pills, feces were the main excretion route of alkaloids from Simiao Pills. The total excretion rates of magnoflorine and berberine in normal rats were 4.87% and 56.54%, which decreased to 2.35% and 35.53% in diabetic rats, which had statistical significance(P<0.05). The total excretion rates of phellodendrine, magnoflorine, and berberine in the urine of diabetic rats decreased significantly, which were 53.57%, 60.84%, and 52.78% of those in normal rats, respectively. After 12 h of intragastric administration, the excretion rate of berberine in the bile of diabetic rats increased significantly, which was 253.33% of that of normal rats. In the condition of diabetes, the excretion rate of berberine metabolite, thalifendine significantly decreased in urine and feces, but significantly increased in bile. The total excretion rates of jateorrhizine and palmatine in the urine increased significantly, and t_(1/2) and K_e changed significantly. The results showed that diabetes affected the in vivo process of alkaloids from Simiao Pills, reducing their excretion in the form of prototype drug, affecting the biotransformation of berberine, and ultimately increasing the exposure of alkaloids in vivo, which would be conducive to the hypoglycemic effect of alkaloids. This study provides references for the clinical application and drug development of Simiao Pills in diabetes.

Qualitative and quantitative analysis of the major components in Qinghao Biejia decoction by UPLC-Orbitrap Fusion-MS/MS and UPLC-QQQ-MS/MS and evaluation of their antibacterial activities.

OBJECTIVE: In the present study, the chemical components of Qinghao Biejia decoction (QBD) were qualitatively and quantitatively analyzed using UPLC-Orbitrap Fusion-MS/MS and UPLC-QQQ-MS/MS techniques, followed by identification of each component's origin and evaluation of the antibacterial activity of QBD and its components. METHODS: High-resolution mass spectrometry was used to obtain information on the precise molecular weight, retention time, and fragmentation ion peaks of the compounds used to identify the components of QBD and establish a method for their quantification. In vitro assays including determination of the minimal inhibitory concentration and growth curves were used to assess the antibacterial activity of QBD and its components. RESULTS: A total of 39 components, including fatty acids, phenolic acids, amino acids, flavonoids, coumarins, terpenoids, and alkaloids, were identified by UPLC-Orbitrap Fusion-MS/MS. A high-performance analytical method was also established to quantify 12 components of QBD. The content of mangiferin was relatively high (estimated to be 814 µg/g). The results of the antibacterial assays indicated that mangiferin exhibits antibacterial effects against two strains causing respiratory tract infections. CONCLUSIONS: The present study suggests that mangiferin may serve as a natural compound which shows high antibacterial activity. The results can aid the discovery and analysis of the active antimicrobial components present in QBD and further provide a reference for quality assessment of multi-component herbal prescriptions.

Geochemical Significance of Biomarkers in the Methane Hydrate-Bearing Sediments from the Shenhu Area, the South China Sea.

Biomarkers from methane hydrate-bearing sediments can provide vital evidence for microbial activities associated with methanogenesis and their relation to the formation of methane hydrates. However, the former mainly focus on intact polar lipids from these microorganisms, and rarely investigate molecular hydrocarbons such as acyclic isoprenoids and hopanes so far. In this work, the composition of biomarkers in the methane hydrate-bearing sediments in cores SH2B and SH7B from the Shenhu area, the South China Sea (SCS) were identified by gas chromatography-mass spectrometry (GC-MS) and comprehensive two-dimensional gas chromatography/time-of-flight mass spectrometry (GC×GC-TOFMS). The occurrence of unresolved complex mixtures (UCMs) and 25-norhopane indicate that the organic matters in methane hydrate-bearing sediments underwent a high degree of biodegradation. Although specific biomarkers for methanogens were not identified, the UCMs, 25-norhopane, pristane, phytane, and hopanes can still indicate the microbial activities associated with methanogenesis. These molecular signals suggest that diverse microorganisms, particularly methanogens, were quite vigorous in the methane hydrate-bearing sediments. Further, the biomarkers identified in this study can also be steadily detected from deep oil/gas reservoirs. Considering numerous adjacent oil/gas reservoir systems, fault systems, and mud diapers occurred in the SCS, it can be inferred that microbial activities and deep oil/gas reservoirs may have jointly contributed to the formation of methane hydrate deposits in the SCS.

Hypoxia induces peroxisome proliferator-activated receptor γ expression via HIF-1-dependent mechanisms in HepG2 cell line.

Hypoxia-inducible factor-1 (HIF-1) can activate expression of a broad range of genes in response to hypoxia. It has been shown that the levels of peroxisome proliferator-activated receptor γ (PPARγ) are influenced by changes in oxygen tension, and PPARγ plays a critical role in metabolism regulation and cancers. In this research, we observed an increased PPARγ mRNA and protein levels in company with increased HIF-1 protein levels in HepG2 cells in hypoxia as compared with in normoxia. Enforced expression of HIF-1α induced PPARγ1 and PPARγ2 expression, while knockdown of HIF-1α by small interference RNA deduced PPARγ1 and PPARγ2 expression in HepG2 cells under hypoxic conditions. By dual-luciferase reporter assay and chromatin immunoprecipitation assay we confirmed a functional hypoxic response element (HRE) localized at 684bp upstream of the transcriptional start site (TSS) of PPARγ1 and a functional HRE localized at 204bp downstream of the TSS of PPARγ2 in HepG2 cells. Additionally we observed an increase and co-presence of PPARγ and HIF-1α, and a highly positive correlation between PPARγ expression and HIF-1α expression (r=0.553, p<0.0001), in the same tumor tissue areas of hepatocellular carcinoma patients. Our data suggested a new mechanism of hepatocellular carcinoma cells response to hypoxia.

Hypoxia-inducible factor-1 (HIF-1) promotes LDL and VLDL uptake through inducing VLDLR under hypoxia.

Metabolism under hypoxia is significantly different from that under normoxia. It has been well elucidated that HIF-1 (hypoxia-inducible factor-1) plays a central role in regulating glucose metabolism under hypoxia; however, the role of HIF-1 in lipid metabolism has not yet been well addressed. In the present study we demonstrate that HIF-1 promotes LDL (low-density lipoprotein) and VLDL (very-LDL) uptake through regulation of VLDLR (VLDL receptor) gene expression under hypoxia. Increased VLDLR mRNA and protein levels were observed under hypoxic or DFO (deferoxamine mesylate salt) treatment in MCF7, HepG2 and HeLa cells. Using dual-luciferase reporter and ChIP (chromatin immunoprecipitation) assays we confirmed a functional HRE (hypoxia-response element) which is localized at +405 in exon 1 of the VLDLR gene. Knockdown of HIF1A (the α subunit of HIF-1) and VLDLR, but not HIF2A (the α subunit of HIF-2), attenuated hypoxia-induced lipid accumulation through affecting LDL and VLDL uptake. Additionally we also observed a correlation between HIF-1 activity and VLDLR expression in hepatocellular carcinoma specimens. The results of the present study suggest that HIF-1-mediated VLDLR induction influences intracellular lipid accumulation through regulating LDL and VLDL uptake under hypoxia.

Combinational study with network pharmacology, molecular docking and preliminary experiments on exploring common mechanisms underlying the effects of weijing decoction on various pulmonary diseases.

Objective: 'Homotherapy for heteropathy' is a theory by which different diseases with similar pathogenesis can be treated with one Chinese formula. We aimed to explore the key components and core targets of Weijing decoction (WJD) in treating various lung diseases, namely, pneumonia, chronic obstructive pulmonary disease (COPD), acute lung injury (ALI), pulmonary fibrosis, pulmonary tuberculosis and non-small cell lung cancer (NSCLC), via network pharmacology, molecular docking and some experiments. Significance: This is the first study on the mechanism of WJD in treating various lung diseases by 'homotherapy for heteropathy'. This study is helpful for the transformation of TCM formula and development of new drugs. Methods: Active components and therapeutic targets of WJD were obtained via TCMSP and UniProt databases. Targets of the six pulmonary diseases were harvested from the GeneCards TTD, DisGeNet, UniProt and OMIM databases. Drug-disease intersection targets, corresponding Venn diagrams, herb-component-target networks and protein-protein interaction networks were established. Furthermore, GO biological function and KEGG enrichment analysis were completed. Moreover, the binding activity between main compounds and core targets was measured through molecular docking. Finally, the xenograft NSCLC mouse model was established. Immune responses were evaluated by flow cytometry and mRNA expression levels of critical targets were measured by real-time PCR. Results: JUN, CASP3 and PTGS2 were the most critical targets in six pulmonary diseases. The active compounds beta-sitosterol, tricin and stigmasterol stably bound to many active sites on target proteins. WJD had extensive pharmacological regulation, involving pathways related to cancer, inflammation, infection, hypoxia, immunity and so on. Conclusions: Effects of WJD against various lung diseases involve lots of compounds, targets and pathways. These findings will facilitate further research as well as clinical application of WJD.

Hypoxia-inducible factor 1-mediated human GATA1 induction promotes erythroid differentiation under hypoxic conditions.

Hypoxia-inducible factor promotes erythropoiesis through coordinated cell type-specific hypoxia responses. GATA1 is essential to normal erythropoiesis and plays a crucial role in erythroid differentiation. In this study, we show that hypoxia-induced GATA1 expression is mediated by HIF1 in erythroid cells. Under hypoxic conditions, significantly increased GATA1 mRNA and protein levels were detected in K562 cells and erythroid induction cultures of CD34(+) haematopoietic stem/progenitor cells. Enforced HIF1α expression increased GATA1 expression, while HIF1α knockdown by RNA interference decreased GATA1 expression. In silico analysis revealed one potential hypoxia response element (HRE). The results from reporter gene and mutation analysis suggested that this element is necessary for hypoxic response. Chromatin immunoprecipitation (ChIP)-PCR showed that the putative HRE was recognized and bound by HIF1 in vivo. These results demonstrate that the up-regulation of GATA1 during hypoxia is directly mediated by HIF1.The mRNA expression of some erythroid differentiation markers was increased under hypoxic conditions, but decreased with RNA interference of HIF1α or GATA1. Flow cytometry analysis also indicated that hypoxia, desferrioxamine or CoCl(2) induced expression of erythroid surface markers CD71 and CD235a, while expression repression of HIF1α or GATA1 by RNA interference led to a decreased expression of CD235a. These results suggested that HIF1-mediated GATA1 up-regulation promotes erythropoiesis in order to satisfy the needs of an organism under hypoxic conditions.

Network Pharmacology-Based Exploration on the Intervention of Qinghao Biejia Decoction on the Inflammation-Carcinoma Transformation Process of Chronic Liver Disease via MAPK and PI3k/AKT Pathway.

Chronic liver disease(CLD) is a slow-developing and long-term disease that can cause serious damage to the liver. Thus far, it has been associated with viral hepatitis, non-alcoholic fatty liver disease(NAFLD), alcoholic liver disease(ALD), hepatic fibrosis(HF), liver cirrhosis (LC), and liver cancer. Qinghao Biejia Decoction (QBD) is a classic ancient Chinese herbal prescription with strong immune-enhancing, anti-inflammatory, and anti-tumor effects. In this study, we used a network pharmacology approach to investigate the molecular mechanisms of QBD in the inflammation-carcinoma transformation process of chronic liver disease. Two key drug targets, MAPK1 and PIK3CA, were screened using network pharmacology and molecular docking techniques, revealing dihydroartemisinin, artesunate, 12-O-Nicotinoylisolineolone, caffeic acid, and diincarvilone A as active ingredients involved in QBD mechanisms. The main signaling pathways involved were the PI3K-AKT signaling pathway and MAPK signaling pathway. In summary, our results indicated that QBD affects the inflammatory transformation of chronic liver disease through MAPK1 and PIK3CA and signaling pathways MAPK and PI3K/AKT. These data provide research direction for investigating the mechanisms underlying the inflammation-carcinoma transformation process in QBD for chronic liver disease.

Hypoxic induction of human erythroid-specific δ-aminolevulinate synthase mediated by hypoxia-inducible factor 1.

Hypoxia-inducible factor 1 (HIF1) is a heterodimeric basic helix-loop-helix transcription factor that regulates many key genes. δ-Aminolevulinate synthase (ALAS) catalyzes the first and rate-limiting reaction in the heme biosynthetic pathway. In this study, we show that hypoxia-induced expression of erythroid-specific ALAS2 is mediated by HIF1 in erythroid cells. Under hypoxic conditions, significantly increased ALAS2 mRNA and protein levels were detected in K562 cells and erythroid induction cultures of CD34+ hematopoietic stem/progenitor cells. Enforced HIF1α expression increased the level of ALAS2 expression, while HIF1α knockdown by RNA interference decreased the level of ALAS2 expression. In silico analysis revealed three potential hypoxia-response elements (HREs) that are located 611, 621, and 741 bp downstream of the ALAS2 gene. The results from reporter gene and mutation analysis suggested that these elements are necessary for a maximal hypoxic response. Chromatin immunoprecipitation and polymerase chain reaction showed that the HREs could be recognized and bound by HIF1α in vivo. These results demonstrate that the upregulation of ALAS2 during hypoxia is directly mediated by HIF1. We hypothesize that HIF1-mediated ALAS2 upregulation promotes erythropoiesis to satisfy the needs of an organism under hypoxic conditions. This may be accomplished via increased heme levels and an interaction between ALAS2 and erythropoietin.

[Repairing front skull base and saddle bottom of cerebrospinal fluid rhinorrhea under endoscopy].

OBJECTIVE: To explore the methods and techniques of repairing cerebrospinal fluid (CSF) rhinorrhea and reconstructing the defects of skull base under endoscopy. METHODS: The clinical data of 26 patients undergoing endoscopic repair of CSF rhinorrhea were analyzed retrospectively. There were 19 males and 7 females with an average age of 31.5 years old. Rhinorrhea was classified into 4 types: ethmoidal sinus type (n = 6), sphenoid sinus type (n = 14) and mixed type (n = 6) and frontal sinus type (n = 0). RESULTS: The causes of rhinorrhea were as follows: traumatic leakage (n = 17), post-operative breakage of saddle area (n = 6), damage after endonasal surgery (n = 2) rhinorrhea after gamma-knife for pituitary (n = 1). All cases were successfully repaired via an endoscopic endonasal approach. Among them, 22 patients were repaired only once while 4 patients with recurrent CSF rhinorrhea were repaired again. The follow-up period was from 6 months to 4 years. And satisfactory outcomes were achieved in all. CONCLUSION: Accurate localization of CSF leakage, reliable reconstruction of skull base, secure fixation of adhesive materials and continuous lumbar CSF drainage are keys surgical techniques. Endoscopic repair of front skull base and saddle bottom of CSF rhinorrhea is a reliable, effective and mini-invasive surgical approach worth further popularization.

Analysis of two sequence variants in peroxisome proliferator activated receptor gamma gene in Tajik population at high altitudes and Han population at low altitudes in China.

The Tajik people in China have resided at high altitude for thousands of years. We analyzed the Pro12Ala (C > G) polymorphism in exon B and the 161C > T polymorphism in exon 6 of peroxisome proliferator activated receptor gamma gene (PPARG) in Chinese Tajik population living at high altitude and Chinese Han population living at low attitude. Significant higher frequencies of the CG and GG genotypes and G allele of the Pro12Ala (C > G) polymorphism were observed in the Tajik population than that in the Han population (P < 0.0001), which suggested the G allele was associated with high-altitude adaptation in the dominate model. The significant differences were remained in both of the male and female groups after stratified by gender, and the differences were more pronounced in men (G versus C, OR = 7.700) than in women (OR = 5.056). No significant difference was observed for the 161C > T polymorphism in the two populations. The frequencies of haplotypes GT (P < 0.0001) and GC (P < 0.05) were significantly higher, while the frequency of CT (P < 0.0001) was significantly lower in the Tajik population than that in the Han population. Our results suggest that PPARG is a candidate gene for high-altitude adaptation in the Chinese Tajik population.

Analysis of two sequence variants in peroxisome proliferator-activated receptor gamma gene in a Tibetan population at high altitude and a Han population at low altitude in China.

BACKGROUND: The Tibetan people in China have lived at high altitude for thousands of years, raising the possibility that the Tibetans are genetically adapted to high altitude. In this study we analyzed the Pro12Ala (C>G) polymorphism in exon 2 and the 161C>T polymorphism in exon 6 of peroxisome proliferator-activated receptor gamma gene (PPARγ) in a Tibetan population and a Han population. MATERIAL/METHODS: We recruited 142 Tibetan volunteers who are permanent inhabitants in Qingzang plateau (higher elevation) and 266 Han volunteers who are permanent inhabitants in the plain (lower elevation). PCR/RFLP method was applied to examine the 2 polymorphisms in the 2 populations. RESULTS: Significantly higher Pro12Ala (C>G) CC genotype frequency and 161C>T CC genotype frequency were observed in the Tibetan population compared to the Han population (p<0.001). When the samples were stratified by sex, significant differences were only observed in females. The haplotypes constructed by Pro12Ala (C>G) and 161C>T were also analyzed. The frequency of the haplotype CC (p<0.0001) was significantly higher, while the frequency of the haplotype CT (p<0.0001) and GT (p<0.01) was significantly lower in the Tibetan population than in the Han population. CONCLUSIONS: Our results suggested that PPARγ might be a candidate gene for high-altitude adaptation; the Pro12Ala (C>G) CC genotype and/or the 161C>T CC genotype are possibly advantageous factors in the female Tibetan population. Alternatively, the difference of the Pro12Ala (C>G) genotype distribution and /or the difference of the 161C>T genotype distribution in the 2 populations may be due to the racial difference.

Polishing of Silicon Nitride Ceramic Balls by Clustered Magnetorheological Finish.

In this study, a novel finishing method, entitled clustered magnetorheological finish (CMRF), was proposed to improve surface finish of the silicon nitride ( Si 3 N 4 ) balls with ultra fine precision. The effects of different polishing parameters including rotation speeds, eccentricities and the machining gaps on surface finish of Si 3 N 4 balls were investigated by analyzing the roughness, sphericity and the micro morphology of the machined surface. The experimental results showed that the polishing parameters significantly influenced the surface finish. The best surface finish was obtained by using the polishing parameters: the machining gap of 0.8 mm, the eccentricity of 10 mm and the rotation ratio of 3/4. To further investigate the influence of the polishing parameters on the surface finish, an analytical model was also developed to analyze the kinematics of the ceramic ball during CMRF process. The resulting surface finish, as a function of different polishing parameters employed, was evaluated by analyzing the visualized finishing trace and the distribution of the contact points. The simulative results showed that the distribution and trace of the contact points changed with different polishing parameters, which was in accordance with the results of experiments.

(3R)-5,6,7-trihydroxy-3-isopropyl-3-methylisochroman-1-one inhibited osteosarcoma growth by inducing apoptosis.

As one of the leading causes of cancer-associated mortalities worldwide, the overall survival rate of osteosarcoma has stably remained at 15-30% for several decades. (3R)- 5,6,7-trihydroxy-3-isopropyl-3-methylisochroman-1-one (TIM), isolated from the whole plant of Selaginella moellendorffii Hieron., has been reported to have pharmacological activities. In the present study, the anti-proliferative effects of TIM against osteosarcoma were evaluated, and the underlying molecular mechanisms were explored. The results demonstrated that TIM inhibited proliferation and induced apoptosis in U2OS cells. Furthermore, the expression of the pro-apoptotic protein NOXA in the intrinsic apoptosis pathway was upregulated by TIM, while the expression of myeloid cell leukemia 1, an anti-apoptotic protein, was downregulated. In addition, TIM increased the protein expression of the endoplasmic reticulum stress markers inositol-requiring enzyme 1, activating transcription factor 6 and glucose-regulated protein 78. These results suggested that TIM induced ER stress response while activating intrinsic apoptosis. Furthermore, treating osteosarcoma tumor-bearing mice with TIM significantly inhibited the tumor growth in the xenograft animal model. Overall, the study results suggested that TIM may serve as a potential antitumor agent against osteosarcoma.

Safety and efficacy of intracoronary human umbilical cord-derived mesenchymal stem cell treatment for very old patients with coronary chronic total occlusion.

This study aimed to investigate the safety and feasibility of intracoronary injection of human umbilical cord mesenchymal stem cell to the very old patients with coronary chronic total occlusion. 15 consecutive patients received mesenchymal stem cells from human umbilical cord in epicardial coronary artery supplying collateral circulation. The patients were randomly allocated to low-dose 3x10(6), mid-dose 4x10(6) and high-dose 5x10(6) groups. (99m)Tc single photon emission computed tomography images were obtained at 12 and 24 months. During the 24 month study period, no cases of major cardiac adverse events were reported. None of the patients had coronary care unit admissions hospitalizations further coronary revascularization acute myocardial infarction and death. The patients had a significant reduction of the infarct size and a remarkable rise in left ventricular ejection fraction with respect to secondary outcomes. This study suggested that stem cell transplantation was safe and feasible. The cells can be utilized to improve in the degree of ischemic myocardium, decrease in the infarct size and rise in left ventricular ejection fraction.

Mechanisms of Improvement of Left Ventricular Function by Intracoronary Human Umbilical Cord-Derived Mesenchymal Stem Cell Infusion in Very Old Patients with Coronary Chronic Total Occlusion.

We have evaluated the safety and efficacy of intracoronary human umbilical cord-derived mesenchymal stem cell (hUCMSC) treatment for very old patients with coronary chronic total occlusion. hUCMSCs could improve in the degree of ischemic myocardium, decrease in the infarct size and rise in left ventricular ejection fraction, but the involved mechanisms remain to be fully identified. We analyzed levels of circulating leukocytes, highsensitivity C-reactive protein (hs-CRP), interleukins (ILs), tumor necrosis factor-a (TNF-a), soluble tumor necrosis factor receptor-1 (sTNFR-1), soluble tumor necrosis factor receptor-2 (sTNFR-2), NT-proBNP, BNP, angiotensin 1-7 (Ang1-7), angiotensin II (Ang II) and aldosterone (Ald) in patients with hUCMSC therapy at baseline, 12, and 24 months. Levels of Ang1-7, IL-10, IL-37 and IL-17 were increased at 12 months and 24 months; leukocytes, hs- CRP, IL-1.

Human Recombinant Endostatin Combined with Cisplatin Based Doublets in Treating Patients with Advanced NSCLC and Evaluation by CT Perfusion Imaging.

AIMS: To study the effectiveness of human recombinant endostatin injection (Endostar®) combined with cisplatin doublets in treating advanced non-small cell lung cancer (NSCLC), and to evaluate outcome by CT perfusion imaging. METHODS: From April 2011 to September 2014, 76 patients with advanced NSCLC who were treated with platinum-based doublets were divided into group A (36 patients) and group B (40 patients). Endostar® 15 mg/day was administered 4 days before chemotherapy and combined with chemotherapy from day 5 in group A, and combined with chemotherapy from the first day in Group B. Endostar® in the two groups was injected intravenously for 14 days. RESULTS: Treatment effectiveness in the two groups differed with statistical significance (p<0.05). Effectiveness evaluated by CT perfusion imaging, BF, BV, MTT and PS also demonstrated significant differences (all p<0.05). Adverse reactions in the two groups did not significantly vary (p>0.05). CONCLUSIONS: The response rate with Endostar® administered 4 days before chemotherapy and combined with chemotherapy from day 5 in group A was better than Endostar® combined with chemotherapy from the first day, and CT perfusion imaging could be a reasonable method for evaluation of patient outcomes.

[Sclerotherapy for renal cyst using erythromycin and procaine via renal puncture guided by B-ultrasound: report of 1,000 cases].

Our experience of sclerotherapy for renal cyst injection of erythromycin and procaine via ultrasound-guided renal puncture is reported. The total efficiency reached 96% with low recurrence rate in the 1,000 cases receiving this therapy, suggesting that this approach is a simple, accurate and effective renal cysts with minimized postoperative complications treatment.

Hypoxia-inducible factor 1-mediated regulation of PPP1R3C promotes glycogen accumulation in human MCF-7 cells under hypoxia.

Hundreds of genes can be regulated by hypoxia-inducible factor 1 (HIF1) under hypoxia. Here we demonstrated a HIF1-mediated induction of protein phosphatase 1, regulatory subunit 3C gene (PPP1R3C) in human MCF7 cells under hypoxia. By mutation analysis we confirmed the presence of a functional hypoxia response element that is located 229bp upstream from the PPP1R3C gene. PPP1R3C induction correlates with a significant glycogen accumulation in MCF7 cells under hypoxia. Knockdown of either HIF1α or PPP1R3C attenuated hypoxia-induced glycogen accumulation significantly. Knockdown of HIF2α reduced hypoxia-induced glycogen accumulation slightly (but not significantly). Our results demonstrated that HIF1 promotes glycogen accumulation through regulating PPP1R3C expression under hypoxia, which revealed a novel metabolic adaptation of cells to hypoxia.