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Bio-Rad rat cd68
Rat Cd68, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 96/100, based on 3261 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rat+anti+cd68/Rat+anti+Mouse+CD68/pmc13051718-411-41-44
Average 96 stars, based on 3261 article reviews

rat cd68 - by Bioz Stars, 2026-09

96/100 stars

Images

Immunofluorescence:

Article Title: Multiparity exacerbates Aβ accumulation and promotes cellular senescence in a mouse model of amyloidosis.
Article Snippet: Proteins were extracted from cells after 3 days of treatment with 200 nM estradiol (E2) (Sigma Aldrich, E2758), 200 nM progesterone (P4) (MCE, HY-N0437), followed by BCA quantification (Thermo Fisher Scientific, A55864) and western blot analysis. .. Antibodies AR TIC LE IN PR ES S 8 The information of primary antibodies used was as follows: rabbit anti-IBA1 (FUJIFILM Wako Chemicals, 019-19741, PRID: AB_839504), goat anti-IBA1 (Novus, NB100-1028, PRID: AB_3148646, 1:500 for immunofluorescence (IF)), rabbit anti-GFAP (Abcam, ab7260, PRID: AB_305808), rat anti-CD68 (BIO-RAD, MCA1957, PRID: AB_3100585), rat anti-LAMP1 (DSHB, clone 1D4B, PRID: AB_2134500), rabbit anti-PU.1 (CST, 2258S, PRID: AB_2186909), rabbit anti-SYNAPTOPHYSIN (Abcam, ab16659, PRID: AB_443419), rabbit anti-PSD-95 (Invitrogen, 51-6900, PRID: AB_2533914), rabbit anti-BACE1 (CST, 5606S, PRID: AB_1903900), rabbit anti-Amyloid Precursor Protein, C-Terminal (Sigma-Aldrich, A8717, PRID: AB_258409), mouse anti-PSD-95 (1:1000; mouse monoclonal, NeuroMab, 75-028, PRID: AB_2292909), rabbit antiFOSB (1:1000; CST, 2251S, PRID: AB_2106903), rabbit anti-SYNAPTOPHYSIN (1:1000 for WB; Abclonal, A6344, PRID: AB_2766946), rabbit anti-BACE1 (rabbit monoclonal, CST, 5606S, PRID: AB_1903900, 1:1000 for WB, 1:500 for IF), chicken anti-MAP2 (1:5000, Abcam, ab5392, PRID: AB_2138153), rabbit anti-Beta-Actin (1:10000; mouse monoclonal; Proteintech, 66009- 1-Ig, PRID: AB_2687938), rabbit anti-β Tubulin (Proteintech, 10094-1-AP, PRID: AB_2210695, 1:5000 for WB) and mouse anti-GAPDH (ProteinTech, 60004-1-Ig, PRID: AB_2107436, 1:10000 for WB). .. The information of secondary antibodies used was as follows: donkey anti-rabbit IgG (H+L) with Alexa FluorTM 488 (Invitrogen, A-21206, PRID: AB_2535729), donkey anti-rabbit IgG (H+L) with Alexa FluorTM 568 (Invitrogen, A10042, PRID: AB_2534017), donkey anti-rabbit IgG (H+L) with Alexa FluorTM 647 (Invitrogen, A-31573, PRID: AB_2536183), donkey anti-goat IgG (H+L) with Alexa FluorTM 488 (Invitrogen, A-11055, PRID: AB_2534102), donkey anti-goat IgG (H+L) with Alexa FluorTM 568 (Invitrogen, A-11057, PRID: AB_2534104), donkey anti-rat IgG (H+L) with Alexa FluorTM 488 (Invitrogen, A48269, PRID: AB_2893137), donkey anti chicken IgY AR TIC LE IN PR ES S 9 (H+L) highly cross adsorbed secondary antibody, Alexa FluorTM 488 (Invitrogen, A78948, PRID: AB_2921070), all diluted by 10% donkey serum in PBS 1:500 for IF.

Western Blot:

Incubation:

Article Title: Loss of mitochondrial DNA helicase in retinal macroglia drives neovascular retinopathy.
Article Snippet: IB4 was detected by incubation with streptavidinconjugated Alexa Fluor 488 antibodies (1:200; Invitrogen; cat#S32354) overnight at 4 °C. .. For the other stainings, the retinas were incubated with primary antibodies (rabbit anti-IBA1 (1:500; Wako Chemicals; cat#019 19741), rat anti-CD68 (1:40; Bio-Rad; catMCA1957), diluted in blocking solution overnight at 4 °C 12 EMBO Molecular Medicine © The Author(s) (RT for Brn3a staining), and then with the corresponding secondary antibodies overnight at 4 °C (1:800 dilution for donkey anti-rabbit Alexa-fluor 594 for IBA1 (Wako), 1:150 dilution for goat anti-rat Alexa fluor 633 for CD68). ..

Article Title: PLGA Nanoparticle-based Anti-TLR2 scFv Gene Delivery for the Treatment of Alzheimer’s Disease
Article Snippet: .. After blocking, cells were incubated overnight at 4°C with the following primary antibodies: mouse anti-His-Tag (Santa Cruz Biotechnology, Dallas, TX, USA), rabbit anti-Iba1 (1:1,000; Wako, Japan), mouse anti-β-Amyloid, 1-16 (1:1,000; Biolegends, San Diego, CA, USA), rat anti-CD68 (1:1,000; Bio-Rad Laboratories, Herucles, CA, USA), and FITC conjugated goat anti-human IgG FcR (1:200; Jackson ImmunoResearch, West Grove, PA, USA). .. The following day, samples were washed three times in PBS and incubated for 2 h at room temperature with secondary antibodies labeled with FITC, Cy3, Alexa Fluor 647 (1:200; Jackson ImmunoResearch).

Blocking Assay:

Staining:

Article Title: The microglial TREM2 receptor programs hippocampal development in a mouse model of childhood deprivation.
Article Snippet: Sections were washed in TBST buffer [1X Trisbuffer saline (Bio-Rad, cat#1706435), 0.5% Triton X-100 (American Bio, CAS 9002–93-1)] and then blocked with TBST containing 10% normal goat serum (NGS, Jackson ImmunoResearch, 005–000-121). .. To assess microglial phagocytic activity, one pool of slices was stained with rabbit anti-IBA1 (1:500; Wako, Cat. #019–19741), mouse anti-PSD95 (1:100; Merck-Millipore, Cat. #MAB1596), and rat anti-CD68 (1:400; Bio-Rad, Cat. # MCA1957T) overnight at 4◦C in TBST-0.5% Triton X100 with 3% NGS. .. TREM2 expression was determined using rabbit antiIBA1 (1:500; Wako, Cat. #019–19741) and rat anti-TREM2 (1:500, R & D Systems, Cat# MAB17291) overnight at 4◦C in TBST- 0.2% Triton X100 with 3% NGS.

Activity Assay:

Next-Generation Sequencing:

Image Search Results

Involvement of profibrotic macrophages in vascular regeneration after graft implantation in vivo . (a) UMAP of macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (b) Dot plots of profibrotic macrophage marker genes (Ctsd, Spp1, Gpnmb, Lgals3, and Fabp5) expressed in different subgroups of macrophages. (c) Percentage of cluster 2 (C2) macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (d) UMAP of expression of Ctsd, Spp1, Gpnmb, Lgals3, and Fabp5 in macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (e) Immunofluorescence staining of CD68 and CTSD in regenerated aortas across different time points after graft implantation in vivo . L indicates lumens. Arrow heads indicate double positively stained cells. (f) WB results of levels of CTSD and SPP1 in native and regenerated aortas across different time points after graft implantation in vivo and quantification of the levels of CTSD and SPP1. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5).

Journal: Bioactive Materials

Article Title: Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1

doi: 10.1016/j.bioactmat.2026.01.029

Figure Lengend Snippet: Involvement of profibrotic macrophages in vascular regeneration after graft implantation in vivo . (a) UMAP of macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (b) Dot plots of profibrotic macrophage marker genes (Ctsd, Spp1, Gpnmb, Lgals3, and Fabp5) expressed in different subgroups of macrophages. (c) Percentage of cluster 2 (C2) macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (d) UMAP of expression of Ctsd, Spp1, Gpnmb, Lgals3, and Fabp5 in macrophages in native aortas and regenerated aortas across different time points after graft implantation in vivo . (e) Immunofluorescence staining of CD68 and CTSD in regenerated aortas across different time points after graft implantation in vivo . L indicates lumens. Arrow heads indicate double positively stained cells. (f) WB results of levels of CTSD and SPP1 in native and regenerated aortas across different time points after graft implantation in vivo and quantification of the levels of CTSD and SPP1. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5).

Article Snippet: The following primary antibodies were used in this study: APOE (Invitrogen, PA5-78803, 1:200 dilution), COL I (abcam, ab270993, 1:200 dilution), COL III (abcam, ab6310, 1:200 dilution), LUM (abcam, ab252925, 1:200 dilution), elastin (abcam, ab307150, ab307150, 1:200 dilution), eNOS (abcam, ab5589, 1:200 dilution), αSMA (abcam, ab7817, 1:200 dilution), Fibronectin (FN, abcam, ab268020, 1:200 dilution), CTSD (CST, 74089S, 1:200 dilution), CD68 (BioRad, MCA341GA, 1:100 dilution), LRP1 (Invitrogen, PA5-101013, 1:200 dilution), Ki67 (Servicebio, GB111141 , 1:200 dilution), and IGF1 (Invitrogen, MA5-18035, 1:200 dilution).

Techniques: In Vivo, Marker, Expressing, Immunofluorescence, Staining

APOE KO reducing profibrotic macrophage formation during vascular regeneration. (a) UMAP of macrophages in native aortas from WT and Apoe −/− rats, heatmap of C2 scores in the UMAP of macrophages in the native aortas, and percentage of C2 cells in macrophages in the native aortas. UMAP of macrophages in regenerated aortas after graft implantation in WT and Apoe −/− rats, heatmap of C2 scores in the UMAP of macrophages in the regenerated aortas, and percentage of C2 cells in macrophages in the regenerated aortas on Day 30 (b) and Day 90 (c). (d) Immunofluorescence staining of CD68 and CTSD in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe−/− rats. (e) Quantification of CD68 and CTSD double positive cells in regenerated aortas on Day 30 and Day 90. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different samples were analyzed (n = 5). (f) WB results of APOE, CTSD and SPP1 levels in regenerated aortas after graft implantation in WT and Apoe −/− rats for 30 and 90 days. (g) Quantification of levels of APOE, CTSD and SPP1 in regenerated aortas on Day 30 and Day 90. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). (h) WB results of APOE, CTSD and SPP1 levels in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h. (i) Quantification of levels of APOE, CTSD and SPP1 in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h ∗ indicates p < 0.05, ∗∗ indicates p < 0.01, unpaired t -test. For each time point and each group, three different samples were analyzed (n = 3). (j) Immunofluorescence staining of APOE and CD68, CTSD and CD68, SPP1 and CD68, respectively, in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h.

Journal: Bioactive Materials

Article Title: Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1

doi: 10.1016/j.bioactmat.2026.01.029

Figure Lengend Snippet: APOE KO reducing profibrotic macrophage formation during vascular regeneration. (a) UMAP of macrophages in native aortas from WT and Apoe −/− rats, heatmap of C2 scores in the UMAP of macrophages in the native aortas, and percentage of C2 cells in macrophages in the native aortas. UMAP of macrophages in regenerated aortas after graft implantation in WT and Apoe −/− rats, heatmap of C2 scores in the UMAP of macrophages in the regenerated aortas, and percentage of C2 cells in macrophages in the regenerated aortas on Day 30 (b) and Day 90 (c). (d) Immunofluorescence staining of CD68 and CTSD in regenerated aortas 30 and 90 days after graft implantation in WT and Apoe−/− rats. (e) Quantification of CD68 and CTSD double positive cells in regenerated aortas on Day 30 and Day 90. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different images from five different samples were analyzed (n = 5). (f) WB results of APOE, CTSD and SPP1 levels in regenerated aortas after graft implantation in WT and Apoe −/− rats for 30 and 90 days. (g) Quantification of levels of APOE, CTSD and SPP1 in regenerated aortas on Day 30 and Day 90. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each time point and each group, five different samples from five different animals were analyzed (n = 5). (h) WB results of APOE, CTSD and SPP1 levels in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h. (i) Quantification of levels of APOE, CTSD and SPP1 in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h ∗ indicates p < 0.05, ∗∗ indicates p < 0.01, unpaired t -test. For each time point and each group, three different samples were analyzed (n = 3). (j) Immunofluorescence staining of APOE and CD68, CTSD and CD68, SPP1 and CD68, respectively, in WT and APOE KO macrophages after their culture on PCL scaffolds for 48 h.

Techniques: Immunofluorescence, Staining

APOE/LRP1 interaction promoting profibrotic macrophage formation during vascular regeneration after graft implantation in vivo . (a) Immunoprecipitation (IP) following mass spectrometry (MS) to screen potential receptors of APOE on surfaces of macrophages. (b) Co-immunoprecipitation (Co-IP) to confirm interaction between APOE and LRP1. (c) Immunofluorescence staining of CD68 and LRP1 in regenerated aortas across different time points. (d) Immunofluorescence staining of APOE and LRP1 in WT macrophages 48 h after their culture on PCL scaffolds. (e) WB results of LRP1, APOE, CTSD and SPP1 levels in WT macrophages cultured on tissue culture plates (negative control, NC) or PCL scaffolds (PCL) for 48 h prior to treatment with shRNA ADV-shRNA(NC) or ADV-shRNA(Lrp1) for 24 h. Quantification of levels of LRP1 (f), APOE (g), CTSD (h) and SPP1 (i) in WT macrophages cultured on tissue culture plates or PCL scaffolds treated with shRNA ADV-shRNA(NC) or ADV-shRNA(Lrp1). ∗ indicates p < 0.05, ∗∗ indicates p < 0.01, N.S. indicates non-significant. Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (j) Flow cytometry analysis of CTSD positive cells in WT macrophages cultured on tissue culture plates (negative control, NC) or PCL scaffolds (PCL) for 48 h prior to treatment with ADV-shRNA(NC) or ADV-shRNA(Lrp1) for 24 h and quantification of percentage of CTSD positive cells in WT macrophages in each group. ∗ indicates p < 0.05, Tukey's post-hoc test. For each group, three independent experiments were repeated, and results were analyzed (n = 3).

Journal: Bioactive Materials

Article Title: Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1

doi: 10.1016/j.bioactmat.2026.01.029

Figure Lengend Snippet: APOE/LRP1 interaction promoting profibrotic macrophage formation during vascular regeneration after graft implantation in vivo . (a) Immunoprecipitation (IP) following mass spectrometry (MS) to screen potential receptors of APOE on surfaces of macrophages. (b) Co-immunoprecipitation (Co-IP) to confirm interaction between APOE and LRP1. (c) Immunofluorescence staining of CD68 and LRP1 in regenerated aortas across different time points. (d) Immunofluorescence staining of APOE and LRP1 in WT macrophages 48 h after their culture on PCL scaffolds. (e) WB results of LRP1, APOE, CTSD and SPP1 levels in WT macrophages cultured on tissue culture plates (negative control, NC) or PCL scaffolds (PCL) for 48 h prior to treatment with shRNA ADV-shRNA(NC) or ADV-shRNA(Lrp1) for 24 h. Quantification of levels of LRP1 (f), APOE (g), CTSD (h) and SPP1 (i) in WT macrophages cultured on tissue culture plates or PCL scaffolds treated with shRNA ADV-shRNA(NC) or ADV-shRNA(Lrp1). ∗ indicates p < 0.05, ∗∗ indicates p < 0.01, N.S. indicates non-significant. Tukey's post-hoc test. For each group, three different samples were analyzed (n = 3). (j) Flow cytometry analysis of CTSD positive cells in WT macrophages cultured on tissue culture plates (negative control, NC) or PCL scaffolds (PCL) for 48 h prior to treatment with ADV-shRNA(NC) or ADV-shRNA(Lrp1) for 24 h and quantification of percentage of CTSD positive cells in WT macrophages in each group. ∗ indicates p < 0.05, Tukey's post-hoc test. For each group, three independent experiments were repeated, and results were analyzed (n = 3).

Techniques: In Vivo, Immunoprecipitation, Mass Spectrometry, Co-Immunoprecipitation Assay, Immunofluorescence, Staining, Cell Culture, Negative Control, shRNA, Flow Cytometry

Downregulation of APOE by AAV ameliorating fibrosis during vascular regeneration after graft implantation in vivo . (a) Illustration of a strategy of adventitial delivery of AAV-shRNA(Apoe) to inhibit APOE levels in regenerated aortas after graft implantation in vivo . Two weeks after graft implantation in vivo , AAV-shRNA(Apoe) were injected into the adventitia of the regenerated aortas, which were then harvested for analysis three weeks later. (b) M mode images of ultrasound detection of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. Arrow heads indicate movement of vascular walls. (c) Tensile tests of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (d) Quantification of RI, PI, and compliance of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (e) Quantification of elastic modulus of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (f) H&E, MTC and EVG staining of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (g) Immunofluorescence staining of COL I, COL III, elastin, αSMA, and eNOS in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. L indicates lumens. Arrow heads indicate capillaries. Quantification of adventitia thickness (h), collagen positive areas according to MTC staining (i), elastin positive areas according to EVG staining (j), COL I positive areas (k), COL III positive areas (l), and number of capillaries (m) in adventitial areas of regenerated aortas. (n) Immunofluorescence staining of CTSD and CD68 in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (o) CD68 and CTSD double positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (p) WB results of APOE, CTSD and SPP1 levels in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks and quantification of levels of APOE, CTSD and SPP1 in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (q) Quantification of IGF-1 concentrations in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks by ELISA. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 3).

Journal: Bioactive Materials

Article Title: Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1

doi: 10.1016/j.bioactmat.2026.01.029

Figure Lengend Snippet: Downregulation of APOE by AAV ameliorating fibrosis during vascular regeneration after graft implantation in vivo . (a) Illustration of a strategy of adventitial delivery of AAV-shRNA(Apoe) to inhibit APOE levels in regenerated aortas after graft implantation in vivo . Two weeks after graft implantation in vivo , AAV-shRNA(Apoe) were injected into the adventitia of the regenerated aortas, which were then harvested for analysis three weeks later. (b) M mode images of ultrasound detection of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. Arrow heads indicate movement of vascular walls. (c) Tensile tests of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (d) Quantification of RI, PI, and compliance of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (e) Quantification of elastic modulus of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different images from six different animals were analyzed (n = 6). (f) H&E, MTC and EVG staining of regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (g) Immunofluorescence staining of COL I, COL III, elastin, αSMA, and eNOS in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. L indicates lumens. Arrow heads indicate capillaries. Quantification of adventitia thickness (h), collagen positive areas according to MTC staining (i), elastin positive areas according to EVG staining (j), COL I positive areas (k), COL III positive areas (l), and number of capillaries (m) in adventitial areas of regenerated aortas. (n) Immunofluorescence staining of CTSD and CD68 in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks. (o) CD68 and CTSD double positive cells in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (p) WB results of APOE, CTSD and SPP1 levels in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks and quantification of levels of APOE, CTSD and SPP1 in regenerated aortas. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 6). (q) Quantification of IGF-1 concentrations in regenerated aortas treated with PBS, AAV-shRNA(NC), and AAV-shRNA(Apoe) for 3 weeks by ELISA. ∗∗ indicates p < 0.01, Tukey's post-hoc test. For each group, six different samples from six different animals were analyzed (n = 3).

Techniques: In Vivo, shRNA, Injection, Staining, Immunofluorescence, Enzyme-linked Immunosorbent Assay

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rat cd68 (Bio-Rad)

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