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Jian-Jun Liu

Publications and source records attributed to Jian-Jun Liu.

At least 37 records · Page 2Linked to original sources
PubMed2004

[Osteopontin enhances migratory ability of cultured aortic adventitial fibroblasts from spontaneously hypertensive rats].

Migration of adventitial fibroblasts (AF) is involved in the neointimal formation which is one of the common pathological processes in several vascular diseases. The observation of whether the migratory response of AF from hypertensive animal is different from that of controls may provide an explanation of vascular remodeling in hypertension. We examined whether there is any difference between the migratory activity of AF derived from spontaneously hypertensive rat (SHR) and that from their normotensive counterpart Wistar-Kyoto rats (WKY). In addition, the role of osteopontin (OPN) in cell migration was also examined. Primary cultures of aortic adventitial fibroblasts were derived from SHR and age-matched WKY. Migration of fibroblasts was determined with the Transwell method. The mRNA expression level of OPN was measured by a real-time quantitative PCR. When compared with WKY-derived cells, migration of adventitial fibroblasts from SHR exhibited an increased response when stimulated by 10% serum (cell number per field 35.20+/-5.26 vs 22.2+/-3.27, p<0.05). Chemotaxis induced by 10 ng/ml bFGF showed a similar difference (cell number per field 30.23+/-4.54 vs 19.20+/-4.47, p<0.05). We also found that SHR-derived fibroblasts expressed a higher level of OPN mRNA than the cells from WKY (1863.23+/-43.91 vs 326.24+/-68.29, p<0.01). To verify if OPN is associated with the enhanced migratory ability in AF from SHR, we designed the antisense oligonucleotide of OPN. The results showed that the antisense OPN oligonucleotide significantly inhibited AF migration (cell number per field 38.60+/-5.98 vs 26.61+/-3.84, p<0.05), while sense and mismatch OPN oligonucleotide had no effect on cell migration. Therefore, the migration of adventitial fibroblasts appeared to be enhanced in cultures derived from SHR. OPN might be involved in the difference observed.

Animals↗
PubMed2004

Heparin/heparan sulfate interacting protein plays a role in apoptosis induced by anticancer drugs.

Heparin/heparan sulfate interacting protein (HIP, also known as ribosome protein L29) is involved in cell-cell and cell-extracellular matrix interactions and influences cell proliferation, migration and differentiation. In the present study, we investigated the role of HIP in anticancer drug-induced apoptosis. Both colon cancer HCT-116 and HT-29 cells showed dose-dependent down-regulation of HIP expression when treated with sodium butyrate. The down-regulation was negatively correlated with the percentage of apoptotic cells (R = -0.955, P = 0.03 and R = -0.792, P = 0.06 for HCT-116 and HT-29 cells, respectively). The correlation between HIP expression and apoptosis in HCT-116 cells was also evident in the differential expression of HIP in the floating and adherent cell populations. Most apoptotic cells were distributed in the floating population. HIP expression in this population was approximately 30% lower than adherent and untreated control cells. HIP expression in HCT-116 cells was also significantly decreased in parallel with apoptosis after treatment with 50 micro M camptothecin and 20 micro M 5-fluorouracil. This indicates that the down-regulation of HIP may be a general phenomenon in anticancer drug-induced apoptosis. The down-regulation of HIP occurred in the early phase of apoptosis, in parallel with the activation of caspase-3 and the externalization of phosphatidylserine. The functional significance of HIP in apoptosis was shown by knocking down the expression of HIP using small interfering RNA. A 50% reduction in HIP expression was sufficient to increase the percentage of apoptotic cells (from 11 to 20%) and increase the sensitivity of the cells to apoptosis induced by 1 mM butyrate by 60%. These results indicate that HIP may play an important role in anticancer drug-induced apoptosis.

Antineoplastic Agents↗
PubMed2004

Protease domain of human ADAM33 produced by Drosophila S2 cells.

Human ADAM33 is a multiple-domain, type-I transmembrane zinc metalloprotease recently implicated in asthma susceptibility [Nature 418 (2002) 426]. To provide an active protease for functional studies, expression of a recombinant ADAM33 zymogen (pro-catalytic domains, pro-CAT) was attempted in several insect cells. The pro-CAT was cloned into baculovirus under the regulation of the polyhedron promoter and using either the honeybee mellitin or ADAM33 signal sequence. Sf9 or Hi5 cells infected with these recombinant viruses expressed the majority of the protein unprocessed and as inclusion bodies ( approximately 10 mg/L). On the other hand, similar constructs could be expressed, processed, and secreted by Drosophila S2 cells using a variety of constitutive (actin, pAc5.1) or inducible (metallothionein, PMT) promoters and leader sequences (e.g., native and BiP). Higher expression level of 10-fold was observed for the inducible system resulting in an average yield of 20 mg/L after purification. The majority of the catalytic domain purified from the Drosophila conditioned media remained associated with the pro-domain after several chromatography steps. An induction cocktail containing cadmium chloride and zinc chloride was subsequently developed for the PMT system as an alternative to using cupric sulfate or cadmium chloride as single inducers. The novel induction cocktail resulted in an increased ratio of secreted catalytic to pro-domain, and yielded milligram amounts of highly purified protease. The availability of this modified expression system facilitated purification of the wild type and several glycosylation mutants, one of which (N231Q) crystallized recently for X-ray structure determination [J. Mol. Biol. 335 (2003) 129].

ADAM Proteins↗
PubMed2004

[Analysis on the relationship between tuberculosis case detection and short-course coverage of directly observed treatment in China].

OBJECTIVE: To analyze factors influencing tuberculosis (TB) case detection so as to predict the trend of case detection in the year of 2005. METHODS: Data was collected and analyzed regarding the correlation between the registration rate of newly identified smear-positive TB case and the directly observed treatment short-course (DOTS) coverage from 1996 to 2003. Based on the correlation analysis, regression equation was built to predict the case registration rate in 2005. RESULTS: Both case registration rate and case detection rate showed an increasing trend from 1996 to 1998 and kept a platform between 1999 and 2002, followed by a zooming change in 2003 to reach a 45% case detection rate while the smear-positive TB case registration rate and DOTS coverage showed highly correlative (r = 0.849, P = 0.008). The regression equation was: y = b(0) + b(1) X = 1.754 + 0.217X (95% CI of beta: 0.082 - 0.352), F = 15.43, P = 0.008; R(2) = 0.72. If the DOTS coverage rate reaches 100% in 2005, the national new smear-positive registration rate will have become 23.5/100 000 (95% CI: 10.0 - 37.0) and the national new smear-positive case detection rate will have reached 51.8% (95% CI: 22.0 - 81.5). CONCLUSION: Our research finding revealed that not only the expansion of DOTS could promote the rate of TB case detection but the quality of DOTS also played an important role in the TB control program. In order to reach the target of 70% case detection rate in 2005, programs as accelerating the DOTS expansion to increase the DOTS coverage and improving the quality of DOTS as well as other control measures need to be strengthened.

China↗
PubMed2004

[Systematic assessment on the improvement of tuberculosis case detection through general hospital-based tuberculosis patients transferring system in China].

OBJECTIVE: To evaluate the reporting and transferring system for tuberculosis (TB) patients carried out by city General Hospitals & township clinics in the last 10 years in China. METHODS: Systematic review and Meta-analysis were carried out. RESULTS: After 5 years of follow-up on the outcomes of intervention, it was found that both the rates of newly registered smear positivity and the new case registration on smear positivity had significantly been increasing during the last five years and the scale of increase was growing annually during the first three years. However, the scale of increase started to decline on the fourth year. The combined RR on the failure of transfer rate was 0.36 (95% CI: 0.25 - 0.53). CONCLUSION: The integrated outcomes showed that the ongoing reporting and transferring system in general hospital was benefit for TB case detection.

China↗
PubMed2004

[Relationship between tuberculosis prevalence and socio-economic factors in China].

OBJECTIVE: In order to figure out how and to what degree the social and economic development and control strategy influencing the epidemics of tuberculosis and to provide reference for tuberculosis prevention and control in China. METHODS: Based on the data from the nationwide random surveys on tuberculosis in 1979, 1984/1985, 1990 and 2000 and the indexes on social and economic development of China, correlation coefficient was used to analyze the relationship of three factors including (1) the change of epidemic situation of tuberculosis from 1979 to 2000; (2) the level of social and economic development; (3) the implementation of Health V Project. RESULTS: The prevalence rate of smear positive tuberculosis was significantly correlated to per capita net income of rural population, consumption level of city population, per capita GDP, density of population, and proportion of rural population. Among which the correlation with per capita net in come of rural population, consumption level of city population, per capita GDP, or density of population showed negative, correlation but the proportion of rural population showed positive. The range of GDP increase was similar in both areas with or without the implementation of Health V Project from 1990 to 2000 (77.2% and 77.8%). However, the ranges of the decline of prevalence rate were quite different (44.4% and 12.3%) in the two areas. In the western part of China, the range of GDP increase was similar in the areas with or without the implementation of Health V Project. However, the prevalence rate declined in the area that implementing the project but increased in other areas without the project. CONCLUSION: The level of social and economic development had influenced the prevalence rate of tuberculosis, but the implementation of tuberculosis control project played an important role in the reduction of tuberculosis prevalence rate from 1979 to 2000 in China.

China↗
PubMed2003

Purification, localization, and expression of human intestinal alkaline sphingomyelinase.

Sphingomyelin (SM) metabolism in the gut may have an impact on colon cancer development. In this study, we purified alkaline sphingomyelinase (alk-SMase) from human intestinal content, and studied its location in the mucosa, expression in colon cancer, and function on colon cancer cells. The enzyme was purified by a series of chromatographies. The molecular mass of the enzyme is 60 kDa, optimal pH is 8.5, and isoelectric point is 6.6. Under optimal conditions, 1 mg of the enzyme hydrolyzed 11 mM SM per hour. The properties of the enzyme are similar to those of rat intestinal alk-SMase but not to those of bacterial neutral SMase. Immunogold electronmicroscopy identified the enzyme on the microvillar membrane in endosome-like structures and in the Golgi complexes of human enterocytes. The expression and the activity of the enzyme were decreased in parallel in human colon cancer tissues compared with the adjacent normal tissue. The enzyme inhibited DNA biosynthesis and cell proliferation dose dependently and caused a reduction of SM in HT29 cells. Intestinal alk-SMase is localized in the enterocytes, down-regulated in human colon cancer, and may have antiproliferative effects on colon cancer cells.

Apoptosis↗
PubMed2003

Differentiation of endothelial progenitor cells from human umbilical cord blood CD 34+ cells in vitro.

AIM: To study the time course of the expression of stem cell marker and endothelial cell markers on human cord blood CD34+ cells during in vitro differentiation process of endothelial progenitor cells (EPC). METHODS: CD34+ cells were selected and enriched from human cord blood by magnetically activated cell sorting (MACS), and cultured in dishes coated with or without fibronectin (Fn). Endothelial cells were identified by staining the cells with anti Flk-1 and vWF antibodies. The percentage of AC133+ cells in adherent CD34+ cell population was analyzed by fluorescence-activated cell sorting (FACS). RESULTS: The expression of Flk-1 and vWF on adherent CD34+ cells increased during the culture time, with 27.0 % positive for Flk-1 and negative for vWF at d 3, and 100 % positive for both Flk-1 and vWF at d 7. When cells were cultured in Fn-treated dishes, the percentages of Flk-1 and vWF positive cells increased to 34 % and 47 %, respectively at d 3, and 100 % at d 7. In contrast, the percentages of AC133+ cells among the adherent cell population decreased rapidly, and similar changes occurred in cells cultured in the presence of Fn. CONCLUSION: The gradual appearance of endothelial cell markers and the disappearance of stem cell marker characterized the in vitro differentiation of endothelial progenitor cells. Fibronectin accelerated the differentiation process of EPC.

AC133 Antigen↗
PubMed2003

Mechanism underlying enhanced endothelium-dependent vasodilatation in thoracic aorta of early stage streptozotocin-induced diabetic mice.

AIM: To investigate the mechanism of the enhanced endothelium-dependent vasodilatation in thoracic aorta of the early stage streptozotocin (STZ)-induced diabetic C57BL/6J mice. METHODS: Radioimmunity was used to detect the metabolite of prostaglandin I2 (PGI2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), in the blood serum. Vascular muscle tension and phenylephrine (PE)-induced rhythmic activity in the isolated thoracic aorta of mice were also compared. RESULTS: 6-Keto-PGF1 alpha in the serum was significantly higher in STZ-induced diabetic mice than age-matched controls [(1.8+/-1.0) microg./L vs (0.5+/-0.3) microg/L, P<0.01]. PE induced rhythmic activity in both diabetic and control mouse aorta but the amplitude was markedly higher in diabetic mice than in controls [(4.9+/-1.7) % vs (12+/-5) %, P<0.01]. PE, high K+ solution-induced contraction, and acetylcholine (ACh)-induced relaxation [(56+/-10) % vs (81+/-8) %, P<0.01] were notably enhanced in diabetic mice than those in controls. Alone NG-nitro-L-arginine methyl ester (L-NAME) or 6-(phenylamino)-5,8-quinolinedione (LY-83583) abolished the rhythmic activity and ACh-induced relaxation in controls but only partially inhibited them in diabetic mice. Indomethacin did not affect rhythmic activity but depressed ACh-induced relaxation. L-NAME plus indomethacin significantly depressed the rhythmic activity and ACh-induced relaxation than L-NAME alone (P<0.01). Furthermore tetraethylammonium plus L-NAME abolished them in diabetic mice. CONCLUSION: The mechanism that enhanced endothelium-dependent vasodilatation in STZ-induced diabetic mice is due to enhanced production of PGI2 and endothelium-derived hyperpolarizing factor (EDHF). The phenomena maybe only take place in early stage of diabetic mice.

6-Ketoprostaglandin F1 alpha↗
PubMed2002

Theoretical study on the mechanism of the 1CHCl + NO reaction.

The complex doublet potential energy surface of the CHClNO system, including 31 minimum isomers and 84 transition states, is investigated at the QCISD(T)/6-311G(d, p)//B3LYP/6-31G(d, p) level in order to explore the possible reaction mechanism of the singlet CHCl with NO. Various possible isomerization and dissociation channels are probed. The initial association between 1CHCl and NO at the terminal N-site can almost barrierlessly lead to the chainlike adducts HClCNO a (a1, a2) followed by the direct Cl-extrusion to product P9 Cl + HCNO, which is the most feasible channel. Much less competitively, a (a1, a2) undergoes a ring-closure leading to the cyclic isomer c-C(HCl)NO d followed by a concerted Cl-shift and N-O cleavage of d to form the branched isomers ClNC(H)O f (f1, f2). Eventually, f (f1, f2) may take a direct H-extrusion to produce P7 H + ClNCO or a concerted 1,2-H-shift and Cl-extrusion to form P1 Cl + HNCO. The low-lying products P2 HCl + NCO, P3 Cl + HOCN, P14 HCO + 3NCl, P6 ClO + HCN, and P13 ClNC + OH may have the lowest yields observed. Our calculations show that the product distributions of the title reaction are quite different from those of the analogous 1CHF + NO reaction, yet are similar to those of another analogous 3CH2 + NO reaction. The similarities and discrepancies among the three reactions are discussed in terms of the substitution effect. The present article may assist in future experimental identification of the product distributions for the title reaction and may be helpful for understanding the halogenated carbene chemistry.

Journal Article↗
PubMed2002

Theoretical study on the mechanism of the (3)CH(2) + NO(2) reaction.

The complex doublet potential energy surface of the CH(2)NO(2) system is investigated at the B3LYP/6-31G(d,p) and QCISD(T)/6-311G(d,p) (single-point) levels to explore the possible reaction mechanism of the triplet CH(2) radical with NO(2). Forty minimum isomers and 92 transition states are located. For the most relevant reaction pathways, the high-level QCISD(T)/6-311 + G(2df,2p) calculations are performed at the B3LYP/6-31G(d,p) geometries to accurately determine the energetics. It is found that the top attack of the (3)CH(2) radical at the N-atom of NO(2) first forms the branched open-chain H(2)CNO(2) a with no barrier followed by ring closure to give the three-membered ring isomer cC(H(2))ON-O b that will almost barrierlessly dissociate to product P(1) H(2)CO + NO. The lesser followed competitive channel is the 1,3-H-shift of a to isomer HCN(O)OH c, which will take subsequent cis-trans conversion and dissociation to P(2) OH + HCNO. The direct O-extrusion of a to product P(3) (3)O + H(2)CNO is even much less feasible. Because the intermediates and transition states involved in the above three channels are all lower than the reactants in energy, the title reaction is expected to be rapid, as is consistent with the measured large rate constant at room temperature. Formation of the other very low-lying dissociation products such as NH(2) + CO(2), OH + HNCO and H(2)O + NCO seems unlikely due to kinetic hindrance. Moreover, the (3)CH(2) attack at the end-O of NO(2) is a barrier-consumed process, and thus may only be of significance at very high temperatures. The reaction of the singlet CH(2) with NO(2) is also briefly discussed. Our calculated results may assist in future laboratory identification of the products of the title reaction.

Journal Article↗
PubMed2002

In vitro effects of fat, FA, and cholesterol on sphingomyelin hydrolysis induced by rat intestinal alkaline sphingomyelinase.

Dietary sphingomyelin (SM) may have regulatory effects on cell proliferation and tumorigenesis in the colon. Alkaline sphingomyelinase (SMase) is the major enzyme responsible for hydrolysis of SM in the gut. Previously we purified the enzyme and showed that the presence of glycerophospholipids inhibited SM hydrolysis induced by alkaline SMase in vitro. In the present work, we studied the effects of TG, DG, FA, ceramide, and cholesterol on SM hydrolysis catalyzed by purified alkaline SMase. The results showed that both TG (triolein and tristearin) and DG (1,2-dioleoyl-sn-glycerol and 1,2-distearoyl-rac-glycerol) inhibited the activity of alkaline SMase. 1-Monooleoyl-rac-glycerol, 1-monostearoyl-rac-glycerol, stearic acid, oleic acid, linoleic acid, linolenic acid, and arachidonic acid stimulated the activity of alkaline SMase at 0.4-0.8 mM concentrations but inhibited the enzyme at higher concentrations. There was no difference between the effects induced by saturated and unsaturated FA. A short-chain FA such as lauric acid had a stronger stimulatory effect at low concentrations and weaker inhibitory effect at high concentrations than long-chain FA. Choosing linoleic acid as an example, we found that FA had similar effects on both alkaline SMase and neutral SMase. Cholesterol and ceramide when mixed with FA to increase its solubility in bile salt micelles inhibited SMase activity. In conclusion, glycerides, FA, ceramide, and cholesterol influence SM hydrolysis catalyzed by intestinal alkaline SMase. The presence of lipids in the diet may thus influence the course of SM digestion in the gut and thereby the exposure of colon to SM metabolites.

Animals↗
PubMed2002

Boswellic acids trigger apoptosis via a pathway dependent on caspase-8 activation but independent on Fas/Fas ligand interaction in colon cancer HT-29 cells.

Boswellic acids are the effective components of gum resin of Boswellia serrata, which has anti-inflammatory properties. Recent studies on brain tumors and leukemic cells indicate that boswellic acids may have antiproliferative and apoptotic effects with the mechanisms being not studied in detail. We studied their antiproliferative and apoptotic effects on colon cancer cells and the pathway leading to apoptosis. HT-29 cells were treated with beta-boswellic acid (BA), keto-beta-boswellic acid (K-BA) and acetyl-keto-beta-boswellic acid (AK-BA), respectively. Apoptosis was determined by flow cytometry, by cytoplasmic DNA-histone complex and the activity of caspase-3. The cleavage of poly-(ADP-ribose)-polymerase (PARP) and expression of Fas were examined by western blot. Specific caspase inhibitors, polyclonal Fas antibody, and antagonistic Fas antibody ZB4 were employed to elucidate apoptotic pathways. DNA synthesis and cell viability were examined. Both K-BA and AK-BA increased cytoplasmic DNA-histone complex dose-dependently and increased pre-G(1) peak in flow cytometer analysis, with the effects of AK-BA being stronger than K-BA. BA only increased the formation of DNA-histone complex at a high concentration. K-BA and AK-BA increased caspase-8, caspase-9 and caspase-3 activities accompanied by cleavage of PARP. The effects of AK-BA on formation of cytoplasmic DNA histone and on caspase-3 activation were 3.7- and 3.4-fold, respectively, more effective than those induced by camptothecin. The apoptosis induced by AK-BA was inhibited completely by caspase-3 or caspase-8 inhibitor and partially by caspase-9 inhibitor. ZB4 blocked exogenous Fas ligand-induced apoptosis, but had no effect on AK-BA-induced apoptosis. AK-BA had no significant effect on expression of Fas. Apart from apoptotic effect, these acids also inhibited [(3)H]thymidine incorporation and cell viability to different extent. In conclusion, boswellic acids, particularly AK-BA and K-BA have antiproliferative and apoptotic effects in human HT-29 cells. The apoptotic effect is mediated via a pathway dependent on caspase-8 activation but independent of Fas/FasL interaction.

Anti-Inflammatory Agents↗
PubMed2002

Hepatic cirrhosis increases sensitivity of kidney to endotoxin in rats.

BACKGROUND: Renal failure in cirrhotic patients is a severe complication and endotoxemia might be involved. We investigated the effect of endotoxin on renal function of cirrhotic rats and the potential protective role of N-acetylcysteine (NAC). MATERIAL/METHODS: Hepatic cirrhosis was generated in a rat model by carbon tetrachloride. Both cirrhotic and normal rats were insulted by endotoxin intravenously, while another cirrhotic group was pre-treated with NAC. Blood urea nitrogen (BUN) and creatinine were assayed eight hours later. The changes in serum tumor necrosis factor-a (TNF-a) were assayed by ELISA. The histological changes in the kidney were observed after hematoxylin and eosin staining. RESULTS: Endotoxin increased the BUN and creatinine levels in both normal and cirrhotic rats, with a much higher elevation in the latter group. TNF-a concentration was also increased by endotoxin; the changes are positively correlated with BUN and creatinine. NAC pretreatment significantly attenuates the effects of endotoxin on BUN, creatinine and TNF-a levels in cirrhotic rats with no improvement in systemic toxicity symptoms. There were no obvious histological changes in the kidney of these animals. CONCLUSIONS: Hepatic cirrhosis increased the sensitivity of renal function to endotoxemia, which may be protected by NAC.

Acetylcysteine↗
PubMed2002

Keto- and acetyl-keto-boswellic acids inhibit proliferation and induce apoptosis in Hep G2 cells via a caspase-8 dependent pathway.

Boswellic acids are the compounds isolated from the gum resin of Boswellia serrata and have been used for the treatment of inflammatory diseases for many years in the countries of the east. Recently, a few studies showed that the acids may have anti-cancer effect on leukemia and brain tumours. We investigated the apoptotic and anti-proliferative effects of two types of boswellic acids, keto-beta-boswellic acid and acetyl-keto-beta-boswellic acid, on liver cancer Hep G2 cells. After treating the cells with the boswellic acids, cell proliferation, DNA synthesis, and apoptosis were analysed. The activities of caspase-3, -8 and -9 were assayed. To explore the apoptotic pathway, specific caspase inhibitors were employed. It was found that boswellic acids decreased cell viability and [3H]thymidine incorporation, checked the cells in the G1 phase, and increased percentage of sub-G1. Boswellic acids strongly induced apoptosis accompanied by activation of caspase-3, -8 and -9. The apoptosis was blocked completely by caspase-8 or caspase-3 inhibitor, but inhibited partly by caspase-9 inhibitor. However, these caspase inhibitors did not show any effect on the alternations of cell viability caused by boswellic acids. In conclusion, boswellic acids have anti-proliferation and anti-cancer effects on Hep G2 cells. The apoptotic effect is mediated by a pathway dependent on caspase-8 activation. The acids may be a promising drug for the chemoprevention of liver cancer.

Anticarcinogenic Agents↗
PubMed2000

A comparison between intravenous and peritoneal route on liver targeted uptake and expression of plasmid delivered by Glyco-poly-l-lysine.

AIM:To compare the effects of intravenous route and peritoneal route on liver targeted uptake and expression of plasmid delivered by galactose-terminal glyco-poly-l-lysine (G-PLL).METHODS:The plasmid pTM/MMP-1 which could be expressed in eukaryotic cells was bound to G-PLL, and was then transferred into Wistar rats by intravenous and intraperitoneal injection. The expression and distribution of the plasmid were observed at different time periods by in situ hybridization and immunohistochemistry.RESULTS:The plasmid could be expressed significantly within 24 h after being transferred in vivo by both intravenous and intraperitoneal routes. One week later the expression began to decrease, and could still be observed three weeks later. Although both the intravenous and intraperitoneal route could target-specifically deliver the plasmid to the liver, the effect of the former was better as compared to that of the latter.CONCLUSION:Intravenous route is better for liver targeted uptake and expression of G-PLL-bound plasmids than the peritoneal route.

Journal Article↗
PubMed2000

Glyco-poly-l-lysine is better than liposomal delivery of exogenous genes to rat of liver.

AIM:To compare the effects of liposomes and glyco-poly-L-lysine on liver targeted uptake and expression of plasmid in rat liver.METHODS:After binding with lipofectamine or galactose-terminal glyco-poly-l-lysine, the plasmid could be expressed in eukaryotic cells when injected in to Wistar rats by intravenous route. At different time intervals after the injection, the distribution and expression of the plasmid in liver of rats were observed and compared using in situ hybridization and immunohistochemistry.RESULTS:The expression of the plasmidbinding to liposomes or G-PLL cou ld be markedly observed 24 h later, and began to decrease one week later,but it still could be observed up to three weeks.Both liposomes and G-PLL coul d deliver the plasmid to the liver effectively, but the effect of the latter was better than the former concerning the distribution and expression of the plasmid targeted uptake in the liver.

Journal Article↗