Biomedical subjects

Hao Ren

Publications and source records attributed to Hao Ren.

At least 19 recordsLinked to original sources

PubMed2006

Induction of haem oxygenase-1 causes cortical non-haem iron increase in experimental pneumococcal meningitis: evidence that concomitant ferritin up-regulation prevents iron-induced oxidative damage.

Desferrioxamine inhibits cortical necrosis in neonatal rats with experimental pneumococcal meningitis, suggesting that iron-induced oxidative damage might be responsible for neuronal damage. We therefore examined the spatial and temporal profile of changes in cortical iron and iron homeostatic proteins during pneumococcal meningitis. Infection was associated with a steady and global increase of non-haem iron in the cortex, particularly in neuronal cell bodies of layer II and V, and in capillary endothelial cells. The non-haem iron increase was associated with induction of haem oxygenase (HO)-1 in neurones, microglia and capillary endothelial cells, whereas HO-2 levels remained unchanged, suggesting that the non-haem iron increase might be the result of HO-1-mediated haem degradation. Indeed, treatment with the haem oxygenase inhibitor tin protoporphyrin (which completely blocked the accumulation of bilirubin detected in HO-1-positive cells) completely prevented the infection-associated non-haem iron increase. The same cells also displayed markedly increased ferritin staining, the increase of which occurred independently of HO activity. At the same time, no increase in DNA/RNA oxidation was observed in infected animals (as assessed by in situ detection of 8-hydroxy[deoxy]guanosine), strongly suggesting that ferritin up-regulation protected the brain from iron-induced oxidative damage. Thus, although pneumococcal meningitis leads to an increase of cortical non-haem iron, protective mechanisms up-regulated in parallel prevent iron-induced oxidative damage. Cortical damage does not appear to be a direct consequence of increased iron, therefore.

Animals↗

PubMed2006

Single quintuple bond [PhCrCrPh] molecule as a possible molecular switch.

The electronic transport properties of a single quintuple bond [PhCrCrPh] molecule sandwiched between two Au(111) surfaces with the trans-bent and linear configurations are studied by a fully self-consistent nonequilibrium Green's function method combined with density functional theory. The calculated transmission spectra of two chemical isomers are remarkably distinctive. Theoretical results suggest that the current through the trans-bent configuration is significantly larger than the corresponding linear one. The predicted on-off ratio of currents ranging from around 50 to 200 in the applied bias window [-1.5 V, 1.5 V] suggests that multiple bond compounds have attractive potential in molecular switch technology.

Journal Article↗

PubMed2006

Mammalian cell entry protein of Mycobacterium tuberculosis induces the proinflammatory response in RAW 264.7 murine macrophage-like cells.

Mammalian cell entry (Mce1A) protein of Mycobacterium tuberculosis (Mtb) is involved in bacterial entry and survival in macrophages, which has been shown to induce production of tumor necrosis factor alpha (TNF-alpha). It remains unclear whether and how Mce1A functions upon the type I interleukin-1 receptor-associated protein kinase (IRAK-1) and TNF receptor-associated factor 6 (TRAF-6) of important proinflammatory cytokines. In this study, His-tagged Mce1A was expressed and purified. Also, two pieces of small interfering RNA (siRNA) were designed and synthesized by in vitro transcription, which exhibit specific and efficient silencing effect on mce1a expression. Furthermore, RAW 264.7 murine macrophage-like cells were exposed to His-tagged Mce1A or co-transfected with the Mce1A-expressing plasmid and efficient siRNA, and levels of IRAK-1 and TRAF-6 were then determined by Western blot. We show here that Mce1A induces up-regulations of IRAK-1 and TRAF-6 in macrophages in a dose-dependent manner. The level of Caspase-3 closely related with apoptosis was also determined, whereas no changes were observed. These results indicate that Mtb Mce1A protein induces a proinflammatory response in macrophages.

Animals↗

PubMed2006

Skp2 contains a novel cyclin A binding domain that directly protects cyclin A from inhibition by p27Kip1.

Skp2 is well known as the F-box protein of the SCF(Skp2) x Roc1 complex targeting p27 for ubiquitylation. Skp2 also forms complexes with cyclin A, which is particularly abundant in cancer cells due to frequent Skp2 overexpression, but the mechanism and significance of this interaction remain unknown. Here, we report that Skp2-cyclin A interaction is mediated by novel interaction sequences on both Skp2 and cyclin A, distinguishing it from the well known RXL-hydrophobic patch interaction between cyclins and cyclin-binding proteins. Furthermore, a short peptide derived from the mapped cyclin A binding sequences of Skp2 can block Skp2-cyclin A interaction but not p27-cyclin A interaction, whereas a previously identified RXL peptide can block p27-cyclin A interaction but not Skp2-cyclin A interaction. Functionally, Skp2-cyclin A interaction is separable from Skp2 ability to mediate p27 ubiquitylation. Rather, Skp2-cyclin A interaction serves to directly protect cyclin A-Cdk2 from inhibition by p27 through competitive binding. Finally, we show that disruption of cyclin A binding with point mutations in the cyclin A binding domain of Skp2 compromises the ability of overexpressed Skp2 to counter cell cycle arrest by a p53/p21-mediated cell cycle checkpoint without affecting its ability to cause degradation of cellular p27 and p21. These findings reveal a new functional mechanism of Skp2 and a new regulatory mechanism of cyclin A.

Amino Acid Motifs↗

PubMed2006

[Effects of peritoneal dialysis solution on proliferation and apoptosis of rat peritoneal mesothelial cells].

OBJECTIVE: To investigate the effects of peritoneal dialysis solution (PDS) on proliferation and apoptosis of rat peritoneal mesothelial cells (RPMCs). METHODS: The proliferation of RPMCs treated with PDS containing glucose of different concentrations for different times in vitro were examined by MTT colorimeric assay. The cell cycles and cell apoptosis rate were determined by flow cytometry. RESULTS: After PDS treatment for 1 h, the cell proliferation inhibition rate, percentage of cells at G(0)/G(1) stage and early cell apoptosis rate increased, and such increment was more manifest with higher glucose concentration in PDS and longer treatment time of the cells. After treatment with PDS containing 4.25% glucose for 3 h, the proliferation inhibition rate of the RPMCs reached 44.12%, the percentage of cells at the G(0)/G(1) stage amounted to 71.95% and the early apoptosis rate reached 23.59%, which was several times higher than that of the negative control and 1.5% glucose/PDS groups, and also higher than that of 4.25% mannitol/PDS groups. CONCLUSION: PDS containing high-concentration glucose can induce significant apoptosis and inhibit the proliferation of RPMCs in vitro.

Animals↗

PubMed2006

[Rapid detection of Pseudomonas aeruginosa by the fluorescence quantitative PCR assay targeting 16S rDNA].

The 16S rDNA specific primers were designed for rapid detection of Pseudomonas aeruginosa (PA) by the fluorescence quantitative PCR (FQ-PCR) assay, based upon multiple sequence alignment and phylogenetic tree analysis of the 16S rDNAs of over 20 bacteria. After extraction of PA genomic DNA, the target 16S rDNA fragment was amplified by PCR with specific primers, and used to construct recombinant pMDT-Pfr plasmid, the dilution gradients of which were subjected to the standard quantitation curve in FQ-PCR assay. Different concentrations of PA genomic DNA were detected by FQ-PCR in a 20microL of reaction system with SYBR Green I. At the same time, various genomic DNAs of Staphylococcus aureus, Salmonella typhi, Shigella flexneri, Proteus vulgaris, Staphylococcus epidermidis, Escherichia coli, and Mycobacterium tuberculosis were used as negative controls to confirm specificity of the FQ-PCR detection assay. Results demonstrated that the predicted amplified product of designed primers was of high homology only with PA 16S rDNA, and that sensitivity of the FQ-PCR assay was of 3.6pg/microL of bacterial DNA or (2.1 x 10(3) +/- 3.1 x 10(2)) copies/microL of 16S rDNA, accompanied with high specificity, and that the whole detection process including DNA extraction could be completed in about two hours. In contrast to traditional culture method, the FQ-PCR assay targeting 16S rDNA gene can be used to detect PA rapidly, which exhibits perfect application prospect in future.

Base Sequence↗

PubMed2006

[Determination of trace manganese by catalytic kinetic spectrophotometry method with CTMAB as the sensitizer].

A new catalytic spectrophotometric method for the determination of trace amount of Mn(II) was developed. The method is based on the oxidation of 7-(2-nitryl-4-methyl phenylazo)-8-hydroxy-qinolin-5-slfonic acid by potassium periodate in the presence of nitrilo triacec acid as an activator and CTMAB as a sensitizer. The wavelengths for the determination was 509 nm. The linear range of determination is 0-3. 2 x 10(-9) g x mL(-1) for Mn(II). The determination limit is 3.8 x 10(-11) g x mL(-1). The interference of foreign ions was studied. The method can be used for the determination of Mn(II) in mung bean, rice, cereal and soil samples.

English Abstract↗

PubMed2005

Hepatitis C virus E2 protein promotes human hepatoma cell proliferation through the MAPK/ERK signaling pathway via cellular receptors.

Dysregulation of mitogen-activated protein kinase (MAPK) signaling pathways by various viruses has been shown to be responsible for viral pathogenicity. The molecular mechanism by which hepatitis C virus (HCV) infection caused human liver diseases has been investigated on the basis of abnormal intracellular signal events. Current data are very limited involved in transmembrane signal transduction triggered by HCV E2 protein. Here we explored regulation of the MAPK/extracellular signal-regulated kinase (MAPK/ERK) signaling pathway by E2 expressed in Chinese hamster oval cells. In human hepatoma Huh-7 cells, E2 specifically activated the MAPK/ERK pathway including downstream transcription factor ATF-2 and greatly promoted cell proliferation. CD81 and low density lipoprotein receptor (LDLR) on the cell surface mediated binding of E2 to Huh-7 cells. The MAPK/ERK activation and cell proliferation driven by E2 were suppressed by blockage of CD81 as well as LDLR. Furthermore, pretreatment with an upstream kinase MEK1/2 inhibitor U0126 also impaired the MAPK/ERK activation and cell proliferation induced by E2. Our results suggest that the MAPK/ERK signaling pathway triggered by HCV E2 via its receptors maintains survival and growth of target cells.

Animals↗

PubMed2005

Hepatitis G virus genomic RNA is pathogenic to Macaca mulatta.

AIM: To explore the pathogenicity and infectivity of hepatitis G virus (HGV) by observing replication and expression of the virus, as well as the serological and histological changes of Macaca mulatta infected with HGV genomic RNA or HGV RNA-positive serum. METHODS: Full-length HGV cDNA clone (HGVqz) was constructed and proved to be infectious, from which HGV genomic RNA was transcribed in vitro. Macaca mulatta BY1 was intra-hepatically inoculated with HGV genomic RNA, HGV RNA-positive serum from BY1 was intravenously inoculated into Macaca mulatta BM1, and then BB1 was infected with serum from BM1. Serum and liver tissue were taken regularly, and checked with RT-PCR, in situ hybridization and other immunological, serological, histological assays. RESULTS: Serum HGV RNA was detectable in all the 3 Macaca mulattas, serological and histological examinations showed the experimental animals had slightly elevated alanine transaminase (ALT) and developed HGV viremia during the infectious period. The histology, immunohis-tochemistry, and in situ hybridization in liver tissues of the inoculated animals demonstrated a very mild hepatitis with HGV antigen expression in cytoplasm of hepatocytes. RT-PCR and quantitative PCR results showed that HGV could replicate in liver. CONCLUSION: The genomic RNA from full-length HGV cDNA is infectious to the Macaca mulatta and can cause mild hepatitis. HGV RNA-positive serum, from HGV RNA inoculated Macaca mulatta, is infectious to other Macaca mulattas. Macaca mulatta is susceptible to the inoculated HGV, and therefore can be used as an experimental animal model for the studies of HGV infection and pathogenesis.

Alanine Transaminase↗

PubMed2005

Immune responses against SARS-coronavirus nucleocapsid protein induced by DNA vaccine.

The nucleocapsid (N) protein of SARS-coronavirus (SARS-CoV) is the key protein for the formation of the helical nucleocapsid during virion assembly. This protein is believed to be more conserved than other proteins of the virus, such as spike and membrane glycoprotein. In this study, the N protein of SARS-CoV was expressed in Escherichia coli DH5alpha and identified with pooled sera from patients in the convalescence phase of SARS. A plasmid pCI-N, encoding the full-length N gene of SARS-CoV, was constructed. Expression of the N protein was observed in COS1 cells following transfection with pCI-N. The immune responses induced by intramuscular immunization with pCI-N were evaluated in a murine model. Serum anti-N immunoglobulins and splenocytes proliferative responses against N protein were observed in immunized BALB/c mice. The major immunoglobulin G subclass recognizing N protein was immunoglobulin G2a, and stimulated splenocytes secreted high levels of gamma interferon and IL-2 in response to N protein. More importantly, the immunized mice produced strong delayed-type hypersensitivity (DTH) and CD8(+) CTL responses to N protein. The study shows that N protein of SARS-CoV not only is an important B cell immunogen, but also can elicit broad-based cellular immune responses. The results indicate that the N protein may be of potential value in vaccine development for specific prophylaxis and treatment against SARS.

Animals↗

PubMed2005

Small interfering RNA-mediated inhibition of hepatitis G virus gene expression in human hepatoma cell Huh-7.

The RNA interference (RNAi) phenomenon is a recently observed process in which the introduction of a double-stranded, small interfering RNA (siRNA) into a cell causes the specific degradation of a homologous single-stranded RNA. It represents an exciting new technology that could have therapeutic applications for the treatment of viral infections. Since hepatitis G virus (HGV) genome is a positive-sense single-stranded RNA, the replication of HGV does not lead to an integrated DNA genome, suggesting a particularly attractive target for RNAi study that could eliminate viral RNA from infected cells. The eukaryotic expression vector pVAX.EH containing the cDNA sequences of the entire HGV structural genes and hygromycin resistance gene downstream from the encephalomyocarditis virus (ECMV) internal ribosome entry site (IRES) was constructed and transfected into human hepatoma cell Huh-7. The modified cleavage products of the structural proteins of HGV expressed in hygromycin-resistant cell line Huh-7-EH were confirmed by RT-PCR and Western blot methods. Two specific HGV E2 siRNAs (1-E2 siRNA, 2-E2 siRNA) synthesized with T7 RNA polymerase by transcription in vitro were transfected into the Huh-7-EH cells. With the analyses of Western blot and the formation of hygromycin-resistant colonies, the inhibitions of expression of HGV structural protein by two HGV E2 siRNAs were detected and found lasting at least one week. The inhibition of 2-E2 siRNA was stronger and only 1% of the cells treated with 2-E2 siRNA formed hygromycin-resistant colonies. These results support that specific HGV 2-E2 siRNAs mediate the degradation of mRNA spanning from HGV structural gene cDNA to hygromycin resistance gene in a majority of cells. In conclusion, the Huh-7-EH cells expressing HGV structural proteins stably can be used as a cell model for studying the replication of HGV and RNAi and the enlargement of RNAi may exist, in mammalian cells.

Antiviral Agents↗

PubMed2005

[Transient cytosolic free calcium changes in cultured neonatal rat cardiac myocytes in response to advanced glycation end-product treatment].

OBJECTIVE: To investigate the effects of advanced glycation end-products (AGEs) on transient cytosolic free calcium in neonatal rat cardiac myocytes (CMs) cultured in vitro. METHODS: CMs cultured for 3 to 5 days in vitro were incubated with Ca(2+)-sensitive fluorescent indicator Fluo-3AM with light screening at 37 degrees celsius; with 5% CO(2) for 60 min. Changes of the fluorescence signal of free calcium caused by AGEs were measured under laser scanning confocal microscope (LSCM). RESULTS: Compared with the control cells, AGEs caused an increase in the concentration of cytosolic free calcium in a dose-dependent manner. CONCLUSION: AGEs may impair neonatal rat CMs by altering cytosolic free calcium concentration.

Aniline Compounds↗

PubMed2005

[Effects of captopril and losartan on expression of kidney aquaporin-2 mRNA and urine aquaporin-2 excretion in rats].

OBJECTIVE: To investigate effects of captopril and losartan on the expression of kidney aquaporin-2 (AQP2) mRNA and the excretion of urine AQP2 in rats. METHODS: Thirty healthy rats were randomized into 3 groups, namely the control group, captopril group and losartan group, respectively. Blood and urine samples were collected from the rats for detecting serum Na(+), urine volume and urine osmolality in the course of medication. Urine AQP2 concentration was measured by enzyme-linked immunosorbent assay (ELISA). Semi-quantitative RT-PCR was performed for measurement of kidney inner medullary AQP2 and vasopressin V(2) receptor mRNA. RESULTS: Urine volume was increased in rats of captopril and losartan groups as compared with that of the control group. However, urine osmolality was lower in captopril group than in the other two groups (P<0.05). RT-PCR revealed decreased quantity of the inner medullary AQP2 mRNA of the captopril group than that of the other two groups, but the quantity of V(2) receptor mRNA did not differ significantly between the 3 groups. Urine AQP2 concentration was significantly higher in captopril group than in the control (P<0.05) and losartan groups (P0<0.01). CONCLUSION: Captopril can reduce the expression of the kidney inner medullary AQP2 mRNA and accelerate the excretion of the urine AQP2 in normal rats.

Angiotensin II Type 1 Receptor Blockers↗

PubMed2004

[Activation of receptor for advanced glycation end products: a mechanism for monocyte-mediated inflammation in chronic renal failure].

OBJECTIVE: To investigate the expression of receptor for advanced glycation end products (RAGE) in chronic renal failure (CRF) and its role in monocyte-mediated inflammation associated with chronic renal failure (CRF). METHODS: Peripheral monocytes (PMC) were isolated from 96 non-diabetic patients with varying severity of CRF. RAGE expression on monocytes was quantitated by flow cytometry. The binding capacity of monocytes with advanced glycation end products (AGE) was determined by 125I-AGEs-HSA binding assay. The plasma level of pentosidine, a marker of AGE, was determined by competitive ELISA. Commercially available kits were used for measuring the plasma levels of neopterin, TNF-alpha and C-reactive protein (CRP), a systemic acute phase reactant. RESULTS: Flow cytometry showed that the RAGE expression at the PMC surface of CRF patients was 8.02 +/- 0.43, significantly higher than that of the normal controls (P < 0.001). The number of functional sites to bind 125I-AGEs-HSA at the surface of PMC of CRF patients was increased in comparison with the normal control group. The biding capacity (Ka) at the surface of PMC of CRF patients was 2 times that of normal control group. Stimulated by AGEs-HAS, the TNF-alpha level in the supernatant of PMC increased dose-dependently in both the normal control and CRF patients, especially in the latter (P < 0.01). After pretreatment of anti-RAGE or non-immune rabbit IgG and then by AGEs-HAS the levels of TNF-alpha in the PMC supernatants of CRF patients and normal controls decreased form 90.52 pg/(10(5) cell) +/- 2.82 pg/(10(5) cell) to 17.86 pg/(10(5) cell) +/- 1.05 pg/(10(5) cell) and from 26.38 pg/(10(5) cell) +/- 1.54 pg/(10(5) cell) to 6.76 pg/(10(5) cell) +/- 0.20 pg/(10(5) cell). HAS not modified by AGEs and non-immune rabbit IgG showed no influence on the secretion of TNF-alpha. The plasma levels of TNF-alpha, neopterin, and CRP increased along with the worsening of renal function. The RAGE expression and pentosidine level at the surface of PMC in CPR patients without hemodialysis were positively correlated with plasma neopterin, TNF-alpha, and CRP levels, even after correction of creatine clearance rate (r = 0.53, P < 0.001; r = 0.58, P < 0.001; r = 0.40, P = 0.001). The expression of RAGE in CRF patients with hemodialysis was positively correlated with the plasma TNF-alpha level (r = 0.33, P = 0.029, n = 36), however, not correlated with neopterin or CRP. CONCLUSION: Enhanced RAGE may trigger a positive feed back loop of AGEs-induced monocyte perturbation, and may contribute to the monocyte-mediated systemic inflammation in CRF.

Adult↗

PubMed2004

Inhibition of EGFP expression by siRNA in EGFP-stably expressing Huh-7 cells.

The RNA interference (RNAi) is a powerful tool to silence gene expression post-transcriptionally, and causes the degradation of an mRNA containing the same sequence. In this present study, an alternative approach was used to in vitro synthesize enhanced green fluorescent protein (EGFP) specific short interfering RNA (siRNA) using T7 RNA polymerase, and a pEGFP-N1 transfected, human hepatoma cell line Huh-7 derived Huh-7-N cell clone was established. When introduced the siRNA into the EGFP expressing Huh-7-N cells, the EGFP specific siRNA was able to specifically inhibit the expression of EGFP in Huh-7-N. In comparison with that in wild-type Huh-7 or that in Huh-7 co-transfected with pEGFP-N1, the inhibition of EGFP specific siRNA in Huh-7-N cells is more significant and repeatable. It is concluded that a cell clone Huh-7-N, which stably expresses EGFP, has been established, and the in vitro synthesized EGFP siRNA can be used in silencing the EGFP gene expression. This Huh-7-N/EGFP specific siRNA system has been proved reliable and convenient, and can also be applied widely as control in other RNA interference studies.

Cell Line↗

PubMed2004

DNA vaccine of SARS-Cov S gene induces antibody response in mice.

The spike (S) protein, a main surface antigen of SARS-coronavirus (SARS-CoV), is one of the most important antigen candidates for vaccine design. In the present study, three fragments of the truncated S protein were expressed in E.coli, and analyzed with pooled sera of convalescence phase of SARS patients. The full length S gene DNA vaccine was constructed and used to immunize BALB/c mice. The mouse serum IgG antibody against SARS-CoV was measured by ELISA with E. coli expressed truncated S protein or SARS-CoV lysate as diagnostic antigen. The results showed that all the three fragments of S protein expressed by E.coli was able to react with sera of SARS patients and the S gene DNA candidate vaccine could induce the production of specific IgG antibody against SARS-CoV efficiently in mice with seroconversion ratio of 75% after 3 times of immunization. These findings lay some foundations for further understanding the immunology of SARS-CoV and developing SARS vaccines.

Animals↗

PubMed2004

Enhanced expression of receptor for advanced glycation end products in chronic kidney disease.

Inappropriate chronic inflammation associated with progressive, chronic kidney disease (CKD) reflects sustained activation of immunocompetent cells, like monocytes/macrophages. Advanced glycation end products (AGE) accumulate in CKD, but it is unclear if they stimulate monocytes by binding with the receptor for AGE (RAGE). Posited was the notion that RAGE plays a contributory role to monocyte-mediated systemic inflammation of progressive CKD. Peripheral blood monocytes were isolated from 102 patients without diabetes with varying severity of CKD. RAGE expression on peripheral blood monocytes increased with worsening CKD (r2 = 0.73) and was strongly correlated with plasma levels of pentosidine, a marker for AGE (r = 0.71). Strongly positive statistical correlations were observed in patients with CKD between monocyte RAGE and plasma levels of tumor necrosis factor alpha (TNF-alpha) (r = 0.61), the monocyte activation marker, neopterin (r = 0.65), and the systemic acute phase reactant, C-reactive protein (r = 0.44). Monocytes obtained from patients with CKD showed a monotonic increase in the number and affinity of specific AGE binding sites and increased production of TNF-alpha under stimulation of AGE. All these upregulatory responses in uremic monocytes could be largely blocked by an anti-RAGE antibody. It was concluded that RAGE expression was upregulated on monocytes from patients with CKD. Enhanced RAGE may amplify AGE-induced monocytes perturbation and contribute to monocyte-mediated systemic inflammation in progressive CKD.

Adult↗

PubMed2004

Clindamycin is neuroprotective in experimental Streptococcus pneumoniae meningitis compared with ceftriaxone.

In animal models of Streptococcus pneumoniae meningitis, rifampin is neuroprotective in comparison to ceftriaxone. So far it is not clear whether this can be generalized for other protein synthesis-inhibiting antimicrobial agents. We examined the effects of the bactericidal protein synthesis-inhibiting clindamycin (n = 12) on the release of proinflammatory bacterial components, the formation of neurotoxic compounds and neuronal injury compared with the standard therapy with ceftriaxone (n = 12) in a rabbit model of pneumococcal meningitis. Analysis of the CSF and histological evaluation were combined with microdialysis from the hippocampal formation and the neocortex. Compared with ceftriaxone, clindamycin reduced the release of lipoteichoic acids from the bacteria (p = 0.004) into the CSF and the CSF leucocyte count (p = 0.011). This led to lower extracellular concentrations of hydroxyl radicals (p = 0.034) and glutamate (p = 0.016) in the hippocampal formation and a subsequent reduction of extracellular glycerol levels (p = 0.018) and neuronal apoptosis in the dentate gyrus (p = 0.008). The present data document beneficial effects of clindamycin compared with ceftriaxone on various parameters linked with the pathophysiology of pneumococcal meningitis and development of neuronal injury. This study suggests neuroprotection to be a group effect of bactericidal protein synthesis-inhibiting antimicrobial agents compared with the standard therapy with beta-lactam antibiotics in meningitis.

Animals↗