tlr4 antagonist lru (InvivoGen)
InvivoGen is a verified supplier 
InvivoGen manufactures this product 
97
Structured Review
InvivoGen
tlr4 antagonist lru
Tlr4 Antagonist Lru, supplied by InvivoGen, used in various techniques. Bioz Stars score: 97/100, based on 1171 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/tlr4+antagonist+lps+rs/LPS-RS+Ultrapure/pm41880679-80-7-12
Average 97 stars, based on 1171 article reviews
Tlr4 Antagonist Lru, supplied by InvivoGen, used in various techniques. Bioz Stars score: 97/100, based on 1171 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/tlr4+antagonist+lps+rs/LPS-RS+Ultrapure/pm41880679-80-7-12
Average 97 stars, based on 1171 article reviews
tlr4 antagonist lru - by Bioz Stars,
2026-10
97/100 stars
Images
Related Articles
Saline:Article Title: Toll-like receptor 4 signaling in trigeminal ganglion neurons contributes tongue-referred pain associated with tooth pulp inflammation. Article Snippet: .. CFA- rats were administered saline (0.5 μL) or Article Title: Toll-like receptor 4 signaling in trigeminal ganglion neurons contributes tongue-referred pain associated with tooth pulp inflammation Article Snippet: .. CFA- rats were administered saline (0.5 μL) or Enzyme-linked Immunosorbent Assay:Article Title: Immunomodulatory activity of polysaccharides isolated from Clerodendrum splendens : Beneficial effects in experimental autoimmune encephalomyelitis Article Snippet: Enzyme-linked immunosorbent assay (ELISA) kits for human tumor necrosis factor (TNF) and granulocyte macrophage-colony stimulating factor (GM-CSF), or human and mouse interleukin (IL)-6 (all from Biolegend) were used to test cytokine protein levels in the cell supernatants. .. Where indicated, PBMCs were pretreated with or without Article Title: Immunomodulatory activity of polysaccharides isolated from Clerodendrum splendens: beneficial effects in experimental autoimmune encephalomyelitis. Article Snippet: Enzyme-linked immunosorbent assay (ELISA) kits for human tumor necrosis factor (TNF) and granulocyte macrophage-colony stimulating factor (GM-CSF), or human and mouse interleukin (IL)-6 (all from Biolegend) were used to test cytokine protein levels in the cell supernatants. .. Where indicated, PBMCs were pretreated with or without other:Article Title: Low Maternal Dietary Intake of Choline Regulates Toll-Like Receptor 4 Expression Via Histone H3K27me3 in Fetal Mouse Neural Progenitor Cells. Article Snippet: Choline is an essential nutrient and a primary dietary source of methyl groups that are vital for brain development.. Low choline (LC) in the maternal diet during pregnancy alters neurogenesis in the foetal brain and leads to low cognitive performance.. However, the key signalling pathways that are sensitive to maternal choline supply during neural progenitor cell (NPC) development and the epigenetic mechanisms by which choline availability regulates gene expression are unclear. Cell Culture:Article Title: Inflammation and joint destruction may be linked to the generation of cartilage metabolites of ADAMTS-5 through activation of toll-like receptors. Article Snippet: .. The SMEs were cultured for 10 days 45 with the given treatments: culture medium only (W/O), OSM (10ng/mL) and TNFα (20ng/mL) in 46 combination (OSM + TNFα), TLR 2/6 agonist - Pam2CSK4 (Invivogen, France, tlrl-pm2s-1) in three 47 doses (100 ng/mL, 10 ng/mL, and 1 ng/mL), TLR1/2 agonist Pam3CSK4 (Invivogen, France, tlrl-pms) 48 in three doses (300 ng/mL, 30 ng/mL and 3 ng/mL), TLR4 agonist - Lipid A (Sigma-Aldrich, USA, L6895) 49 in 3 doses (1000 ng/mL, 100 ng/mL and 1 ng/mL) with or without the |
![Figure 2 Effect of <t>TLR4</t> antisense on preventing and reversing oxaliplatin, paclitaxel and bortezomib CIPN. Top: Groups of male rats were treated intra thecally (i.t.) with antisense (AS)-oligodeoxynucleotides (ODN) or mismatch (MM)-ODN (both 120 μg in 20 μl/day) against TLR4 mRNA, once a day start ing 3 days before (Day −3) each chemotherapy drug, for seven doses, over 10 days. Rats received (A) oxaliplatin [2 mg/kg, intravenously (i.v.), on Day 0]; (B) paclitaxel [1 mg/kg, intraperitoneally (i.p.), on Days 0, 2, 4 and 6]; or (C) bortezomib (0.2 mg/kg, i.v., on Days 0, 2, 4 and 6). The mechanical nociceptive threshold was evaluated before the first intrathecal administration of ODN (Day −3) and then from Days 0 to 28. In the TLR4 antisense-treated rats, CIPN hyperalgesia was markedly inhibited in the oxaliplatin-, paclitaxel- and bortezomib-treated rats (A, B and C, respectively), and this attenuation was undiminished over the 28-day testing period (all data are mean ± SEM). Statistical analyses for (A) oxaliplatin: two-way repeated-measures ANOVA, Time × TLR4 AS-ODN interaction, F(6,60) = 27.22, P < 0.0001; TLR4 AS-ODN treatment, F(1,10) = 210.6, P < 0.0001; Bonferroni's multiple post hoc compar isons test, ****P < 0.0001 (TLR4 MM-ODN versus TLR4 AS-ODN); (B) paclitaxel: two-way repeated-measures ANOVA, Time × TLR4 AS-ODN interaction, F(7,70) = 39.54, P < 0.0001; TLR4 AS-ODN treatment, F(1,10) = 333.2, P < 0.0001; Bonferroni's multiple post hoc comparisons test, ****P < 0.0001, ***P = 0.0001, *P = 0.0299 (TLR4 MM-ODN versus TLR4 AS-ODN); and (C) ortezomib; two-way repeated-measures ANOVA, Time × TLR4 AS-ODN interaction, F(6,60) = 7.817, P < 0.0001; TLR4 AS-ODN treatment, F(1,10) = 280.8, P < 0.0001; Bonferroni's multiple post hoc comparisons test, ****P < 0.0001, ***P = 0.0004 (TLR4 MM-ODN versus TLR4 AS-ODN). n = 6 paws for each group. Bottom: Separate groups of male rats received: (D) oxaliplatin (2 mg/kg, i.v., on Day 0); (E) paclitaxel (1 mg/kg, i.p., on Days 0, 2, 4 and 6); or (F) bortezomib (0.2 mg/kg, i.v., on Days 0, 2, 4 and 6). Each group was then treated intra thecally with AS-ODN or MM-ODN (both 120 μg in 20 μl/day) against TLR4 mRNA once a day starting 3 days after the last dose of chemotherapy agent, for seven doses, over 10 days. The mechanical nociceptive threshold was evaluated from Days 0 to 28. In the TLR4 AS-ODN-treated group, CIPN hyper algesia was markedly attenuated in oxaliplatin- and paclitaxel-treated rats, and this attenuation was undiminished for the 28-day testing period. Bortezomib-induced hyperalgesia was reversed on Day 14, but hyperalgesia returned, after ending antisense administration, on Days 21 and 28. Statistical analyses for (D) oxaliplatin: two-way repeated-measures ANOVA, Time × TLR4 AS-ODN interaction, F(5,50) = 41.94, P < 0.0001; TLR4 AS-ODN treatment, F(1,10) = 67.68, P < 0.0001; Bonferroni's multiple post hoc comparisons test, aaaP = 0.0002, ***P = 0.0008, ****P < 0.0001, cccP = 0.0001 (MM-ODN versus AS-ODN); (E) paclitaxel: two-way repeated-measures ANOVA, Time × TLR4 AS-ODN interaction, F(4,40) = 75.11, P < 0.0001; TLR4 AS-ODN treatment, F(1,10) = 100.6, P < 0.0001; Bonferroni's multiple post hoc comparisons test, ****P < 0.0001 (MM-ODN versus AS-ODN); and (F) borte zomib: two-way repeated-measures ANOVA, Time × TLR4 AS-ODN interaction, F(6,60) = 44.08, P < 0.0001; TLR4 AS-ODN treatment, F(1,10) = 23.6, P = 0.0007; Bonferroni's multiple post hoc comparisons test, ****P < 0.0001 (MM-ODN versus TLR4 AS-ODN at Day 14 after first bortezomib administration). All data are mean ± SEM. n = 6 paws for each group. CIPN = chemotherapy-induced peripheral neuropathy.](https://pub-med-unpaywalled-images-cdn.bioz.com/pub_med_ids_ending_with_7114/pm37787114/pm37787114__page5_image1.jpg)
![Figure 3 TLR4 antisense attenuates TLR4 protein expression in L4 and L5 dorsal root ganglia and oxaliplatin-induced CIPN. Western blot analysis of dorsal root ganglia (DRG) extracts from male rats treated intrathecally with antisense-oligodeoxynucleotides (AS-ODN) against TLR4 mRNA, once a day for 4 days (120 µg in 20 µl/day). (A) TLR4 AS-ODN-treatment significantly decreased anti-TLR4 immunoreactivity 24 h after the last treatment (−28.06 ± 1.29%, unpaired Student's t-test, n = 3, *P < 0.05). Of note, the magnitude of the attenuation of TLR4 in DRG neurons is probably an underestimate, as TLR4 levels in other cells in the DRG are not affected by intrathecal antisense but are measured on the western blots. (B) Nine days after the last ad ministration of TLR4 AS-ODN, anti-TLR4 immunoreactivity was not significantly different from the levels in DRG from TLR4 mismatch (MM)-ODN-treated rats (−2.32 ± 3.6%, unpaired Student's t-test, n = 3, P > 0.05). The calculated molecular weight of TLR4 is 96 kDa (according to UniProtKB database entry Q9QX05). The difference between the calculated and apparent molecular weights may be due to the glycosylation of TLR4. β-Actin, which was used as a loading control, has a calculated molecular weight of ∼42 kDa (according to UniProtKB database entry P60771). The full-length gels and blots are included in Supplementary Fig. 3. (C) Male rats were treated intrathecally with AS-ODN or MM-ODN (both 120 μg in 20 μl/day) against TLR4 mRNA once a day for 4 days consecutively. On Day 0 (9 days after the last intrathecal ODN injection), rats received oxaliplatin [2 mg/kg, intravenously (i.v.)], and the mechanical nociceptive threshold was evaluated before the first intrathecal administration of ODN (Day −12) and then from Days 0 to 28. In the TLR4 AS-ODN-treated group, oxaliplatin did not develop hyperalgesia until Day 28. Two-way repeated-measures ANOVA, Time × TLR4 AS-ODN interaction, F(6,60) = 35.66, P < 0.0001; TLR4 AS-ODN treatment, F(1,10) = 881.1, P < 0.0001; Bonferroni's multiple post hoc comparisons test, ****P < 0.0001 (TLR4 MM-ODN versus TLR4 AS-ODN). n = 6 paws for each group. All data are mean ± SEM. CIPN = chemotherapy-induced peripheral neuropathy.](https://pub-med-unpaywalled-images-cdn.bioz.com/pub_med_ids_ending_with_7114/pm37787114/pm37787114__page6_image1.jpg)
![Figure 4 Intrathecal but not intradermal administration of a TLR4 selective antagonist reverses oxaliplatin, paclitaxel and bortezomib CIPN. Top: Groups of male rats received (A and D) oxaliplatin [2 mg/kg, intravenously (i.v.), on Day 0]; (B and E) paclitaxel [1 mg/kg, intraperitoneally (i.p.), on Days 0, 2, 4 and 6]; or (C and F) bortezomib (0.2 mg/kg, i.v., on Days 0, 2, 4 and 6). The mechanical nociceptive threshold was evaluated on Day 0 before the chemotherapy drug was administered and then at Day 28 after their administration. On Day 28 after chemotherapy drugs, rats received intrader mal vehicle (saline, 5 μl) or TLR4 antagonist (LPS-RS Ultrapure, 3 μg/5 μl), and the mechanical nociceptive threshold was evaluated 30 and 60 min later. Intradermal TLR4 antagonist did not attenuate CIPN hyperalgesia in the oxaliplatin-, paclitaxel- and bortezomib-treated rats (A, B and C, respectively). Statistical analyses for intradermal TLR4 antagonist (A) oxaliplatin: two-way repeated-measures ANOVA, Time × TLR4 antagonist interaction, F(3,12) = 0.749, P = 0.5434; TLR4 antagonist treatment, F(1,10) = 0.347, P = 0.5876; Bonferroni's multiple post hoc comparisons test, not significant (ns; vehicle ver sus TLR4 antagonist); (B) paclitaxel: two-way repeated-measures ANOVA, Time × TLR4 antagonist interaction, F(3,12) = 1.136, P = 0.3738; TLR4 antagon ist treatment, F(1,10) = 2.009, P = 0.3393; Bonferroni's multiple post hoc comparisons test, ns (vehicle versus TLR4 antagonist); and (C) bortezomib: two-way repeated-measures ANOVA, Time × TLR4 antagonist interaction, F(3,12) = 2.157, P = 0.1462; TLR4 antagonist treatment, F(1,10) = 1.382, P = 0.3050; Bonferroni's multiple post hoc comparisons test, ns (vehicle versus TLR4 antagonist). n = 6 paws for each group. Bottom: Separate groups of male rats, treated 28 days prior with (D) oxaliplatin (2 mg/kg, i.v.), (E) paclitaxel (1 mg/kg, i.p.) or (F) bortezomib (0.2 mg/kg, i.v.), received intrathecally vehicle (saline, 20 μl) or TLR4 antagonist (LPS-RS Ultrapure, 10 μg/20 μl), and the mechanical nociceptive threshold was evaluated 30, 60 and 120 min later. In the group treated with intrathecal TLR4 antagonist, oxaliplatin-, paclitaxel- and bortezomib-induced hyperalgesia was markedly attenuated (D, E and F, respectively), and this inhibition was undiminished for the 120-min testing period. Statistical analyses for intrathecal TLR4 antagonist (D) oxaliplatin: two-way repeated-measures ANOVA, Time × TLR4 antagonist interaction, F(4,40) = 74.54, P < 0.0001; TLR4 antagonist treatment, F(1,10) = 168.3, P < 0.0001; Bonferroni's multiple post hoc comparisons test, ****P < 0.0001 (vehicle versus TLR4 antagonist); (E) paclitaxel; two-way repeated- measures ANOVA, Time × TLR4 antagonist interaction, F(4,40) = 73.01, P < 0.0001; TLR4 antagonist treatment, F(1,10) = 216.8, P < 0.0001; Bonferroni's multiple post hoc comparisons test, ****P < 0.0001 (vehicle versus TLR4 antagonist); and (F) bortezomib: two-way repeated-measures ANOVA, Time × TLR4 antagonist interaction, F(4,32) = 32.66, P < 0.0001; TLR4 antagonist treatment, F(1,10) = 30.99, P = 0.0005; Bonferroni's multiple post hoc comparisons test, aP = 0.0341, *P = 0.0248, cP = 0.0252 (vehicle versus TLR4 antagonist). n = 6 paws for each group. All data are mean ± SEM. LPS-RS Ultrapure = lipo polysaccharide from Rhodobacter sphaeroides. CIPN = chemotherapy-induced peripheral neuropathy.](https://pub-med-unpaywalled-images-cdn.bioz.com/pub_med_ids_ending_with_7114/pm37787114/pm37787114__page7_image1.jpg)
![Figure 5 Oxaliplatin-induced nociceptor sensitization, in vitro, is TLR4 dependent. (A) Example traces for the lower (more negative) action potential (AP) threshold in a small dorsal root ganglia (DRG) neuron of an oxaliplatin-treated rat (middle) compared with naïve rats (left), and the lack of such oxaliplatin-induced lowering of the AP threshold after in vivo pretreatment with TLR4 antisense-oligodeoxynucleotides (AS-ODN) in the prevention protocol (right). Traces show APs generated in response to a current step with height equal to rheobase (minimum current required to induce an AP) in three different neurons. The scale is the same for all panels. AP threshold is indicated by short grey tick. Rectangle inset in the upper right corner of each panel shows magnified region of recordings near the position of the AP threshold. Thin light grey line shows fit of the initial phase of the de polarization with a single exponent corresponding to passive charging of the neuron's capacitance. Deviation of the actual neuronal depolarization of 2 mV above the fit was defined as the AP threshold (see the ‘Materials and methods’ section for details). (B) Effect of oxaliplatin administered in vivo on AP threshold, and the attenuation of this effect by TLR4 AS-ODN administered in vivo, in the prevention protocol. Oxaliplatin induced a reduction in the AP threshold compared with the control group [untreated naïve animals; one-way ANOVA: F(2,26) = 6.3, P = 0.006; Holm–Šídák's post hoc test: t(26) = 3.6, **adjusted P = 0.003]. TLR4 AS-ODN administered before oxaliplatin produced a significant shift in the AP threshold back towards the control value [t(26) = 2.1, #adjusted P = 0.04 compared with in vivo oxaliplatin]. (C) Effect of in vitro administration of oxaliplatin on the AP threshold, and its attenu ation by TLR4 AS-ODN administered in vivo, in the prevention protocol. Oxaliplatin (50 μM) induced a significant reduction in the AP threshold (after preincubation for 3 h before recording) compared with the control group [one-way ANOVA: F(2,29) = 10.5, P = 0.0004; Dunnett's post hoc test: q(29) = 4.1, ***adjusted P = 0.0005]. TLR4 AS-ODN administered in vivo, before oxaliplatin, produced a significant shift in the AP threshold back towards the con trol value [Dunnett's post hoc test: q(29) = 3.9, ##adjusted P = 0.0010 compared with in vitro oxaliplatin]. (D) Effect of in vitro administration of LPS-RS Ultrapure, a selective inhibitor of TLR4, on oxaliplatin-induced reduction in AP threshold (‘all in vitro’ prevention). Preincubation of cultured neurons with LPS-RS Ultrapure (10 μg/ml for 24 h) before adding oxaliplatin (for 3 h before and during the recording) significantly shifted the AP threshold back towards the control value compared with the significantly more negative AP threshold observed in in vitro oxaliplatin-treated neurons [one-way ANOVA: F(2,28) = 7.0, P = 0.004; Dunnett's post hoc test: q(25) = 3.7, **adjusted P = 0.0018 for in vitro oxaliplatin, when compared with control; q(28) = 2.4, #adjusted P = 0.04 for LPS-RS Ultrapure, when compared with in vitro oxaliplatin]. (E) Effect of LPS-RS Ultrapure administered in vitro on AP threshold in neurons derived from animals treated with oxaliplatin in vivo (in vitro reversal after in vivo induction of nociceptor sensitization). Incubation of such neurons with LPS-RS Ultrapure (10 μg/ml for 24 h) produced a significant shift in the AP threshold back towards the control value when compared with the significantly more negative AP threshold observed in neurons from oxaliplatin-treated animals [one-way ANOVA: F(2,25) = 9.5, P = 0.0009; Dunnett's post hoc test: q(25) = 3.7, **adjusted P = 0.0019 for in vivo oxaliplatin, when compared with control; q(25) = 3.9, ##adjusted P = 0.0014 for LPS-RS Ultrapure, when compared with in vivo oxaliplatin]. Number of cells: B, C, D and E share the same data set for the control group (left bars), n = 14; B and E share the same data set for the in vivo oxaliplatin group (middle bars), n = 8; C and D share the same dataset for the in vitro oxaliplatin group (middle bars), n = 9. Number of cells in prevention or reversal groups (right bars): n = 7 in B, n = 9 in C, n = 8 in D, n = 6 in E. LPS-RS Ultrapure = lipopoly saccharide from Rhodobacter sphaeroides.](https://pub-med-unpaywalled-images-cdn.bioz.com/pub_med_ids_ending_with_7114/pm37787114/pm37787114__page9_image1.jpg)
![Figure 7 TLR4 and RAGE antisense reverses oxaliplatin CIPN in female rats. Female rats received oxaliplatin [2 mg/kg, intravenously (i.v.)] on Day 0, and 4 days later, they were treated with intrathecal antisense-oligodeoxynucleotides (AS-ODN) or mismatch (MM)/sense (SE)-ODN (both 120 μg in 20 μl/ day) against (A) TLR4 or (B) RAGE mRNA, once a day for 4 days consecutively, and then three more doses, one every other day, for a total of seven doses, over 10 days. The mechanical nociceptive threshold was evaluated from Days 0 to 28. Oxaliplatin-induced hyperalgesia was markedly reversed in the (A) TLR4 and (B) RAGE AS-ODN-treated groups of female rats, and this reversal was undiminished over the 28-day testing period. Statistical analyses for A: two-way repeated-measures ANOVA, Time × TLR4 AS-ODN interaction, F(5,50) = 64.68, P < 0.0001; TLR4 AS-ODN treatment, F(1,10) = 95.41, P < 0.0001; Bonferroni's multiple post hoc comparisons test, ****P < 0.0001 (MM-ODN versus AS-ODN); and B: two-way repeated-measures ANOVA, Time × RAGE AS-ODN interaction, F(5,50) = 77.11, P < 0.0001; RAGE AS-ODN treatment, F(1,10) = 368.2, P < 0.0001; Bonferroni's multiple post hoc comparisons test, ****P < 0.0001 (SE-ODN versus AS-ODN). n = 6 paws for each group. All data are mean ± SEM. CIPN = chemotherapy-induced peripheral neuropathy.](https://pub-med-unpaywalled-images-cdn.bioz.com/pub_med_ids_ending_with_7114/pm37787114/pm37787114__page11_image1.jpg)
