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Cl 1000m

Manufactured by Analytik Jena
Sourced in United States

The CL-1000M is a UV-VIS spectrophotometer designed for precise and reliable absorbance measurements. It features a compact design, a 2 nm bandwidth, and a wavelength range of 190 to 1100 nm. The CL-1000M is a versatile instrument suitable for a variety of analytical applications.

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11 protocols using cl 1000m

1

UVB-Induced Skin Damage in Rats

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The dorsal side of the rats was shaved 24 h before the beginning of the experiment. Sixty rats were randomly divided into six groups, each containing 10 animals: a negative control group (C1) was not exposed to irradiation; a positive control group was subjected daily to UVB irradiation for 10 consecutive days and received no treatment. The other four groups named T1, T2, T3, and T4 received RHE, 4%-RM-LNC gel, 10% RM-LNC gel, and plain LNC gel, respectively, daily one hour before the UVB exposure A UV lighter (peak emission was 302 nm, CL-1000 M, UVP, Upland, CA, USA) was used for UVB irradiation. UVB irradiation doses were 40–80 mJ/cm2 (exposure time was 15–30 s) and the lamp was fixed 5 cm above the platform where rats were placed119 (link).
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2

UVB-Induced Skin Damage and PRE Treatment

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Five-week-old female albino hairless mice (SKH-1) were purchased from Orient Bio Inc. (Gyeonggi-do, Korea). The experimental protocols were approved by the Institutional Animal Care and Use Committee of Yonsei Laboratory Animal Research Center (Permit number: 201509-471-03). Eighteen mice were randomly divided into three groups: (1) normal group, (2) UVB group, and (3) UVB + PRE group. For 8 weeks, mice of the UVB and the UVB + PRE groups were exposed to UVB every alternate day using the UV crosslinker CL-1000M (UVP). The UVB dose started at 75 mJ/cm2. Then, the dose was increased by 1 minimal erythema dose (MED) per week, until 3 MED, which was maintained until end of the experiments. Mice of the UVB + PRE group were orally given 300 mg/kg/day PRE and the remaining groups received saline. After 8 weeks, the mice were anesthetized using 2,2,2-tribromoethanol (Sigma-Aldrich) and sacrificed. For optical microscopy, the dorsal skin samples were fixed in 10% formalin and the residual dorsal skin was stored at −80°C.
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3

UV-Induced Stress Response in Hs68 Cells

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Hs68 cells were cultured and exposed to UV irradiation as previously described [53 (link)]. Cells were incubated in DMEM without serum in the presence of CAE for 24 h after UVB irradiation. A UV lighter (peak emission was 302 nm, CL-1000 M, UVP, Upland, CA, USA) was used for UVB exposure. UVB irradiation doses were 40–80 mJ/cm2 (exposure time was 15–30 s) [32 (link),54 (link)].
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4

UVB-Induced Photoaging Model in Rats

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The UVB irradiation system was utilized to stimulate skin photoaging in mice. A UV radiation source with peak emission at 302 nm (CL-1000 M; UVP, Upland, CA, USA) was used as a UVB irradiation source. The UVB irradiation doses were 40–80 mJ/cm2, with an exposure time of 15–30 s, and the lamp was fixed 5 cm above the platform where rats were placed [63 (link),91 (link)]. Twenty-four hours prior to the experiment, the dorsal side of the rats was shaved. Animals were then divided into five groups (n = 10),
SPR concentration in both SPR suspension and SPR-BS was 1.125% [37 (link)]. At the end of the experiment, about 10 days after the initiation of UVB irradiation, visual observation of the wrinkles in the dorsal side of the rat skin were performed.
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5

Human Foreskin Fibroblasts UVB Exposure

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Human foreskin fibroblasts (Hs68) were incubated in Dulbecco’s modified Eagle’s medium containing 10% fetal bovine serum and 100 U/mL penicillin and streptomycin. The cells were grown in an incubator at 37 °C with 5% CO2. The cells were exposed to UVB in a UV crosslinker (302 nm UV, 5 × 8 watt UV dual bipin discharge type, CL-1000M, UVP, Upland, CA, USA) that delivered a UVB energy of wavelength 302 nm. The UVB dose was 40 mJ/cm2, and the exposure was approximately 15 s.
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6

UVB-Induced Skin Damage Attenuation

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After 1 week of acclimatization, the mice were randomly divided into the following five groups: control, UVB-irradiated and vehicle (PEG-400)-treated, UVB-irradiated and 3% arbutin-treated, UVB-irradiated and 1% sesamol–treated, UVB-irradiated and 3% sesamol–treated groups. Each group consisted of six mice. This study used UV light (broadband with peak emission at 302 nm, CL-1000 M, UVP, USA). The mice were exposed to 180 mJ/cm2 of UVB irradiation three times a week (on days 1, 3, and 5) for 2 weeks according to previous methods with slight modification [23 (link)]. Vehicle-treated UVB-irradiated mice were topically administered PEG on the ear skin daily, and sesamol-treated mice were topically administered 1% or 3% sesamol on the ear skin daily. Sesamol was applied on the skin after UVB irradiation. Control mice did not receive any treatment. Details of the animal experimental process are presented in Figure 1.
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7

UVB-Induced HS68 Cell Response

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At 80% confluence, the medium was substituted with Dulbecco's Phosphate-Buffered Saline (DPBS) and HS68 cells were irradiated with UVB (15 mJ/cm2) using the UV crosslinker CL-1000M (UVP, Cambridge, UK). After washing with DPBS, the cells were treated with DMEM including PRE for an additional 24 h.
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8

UVB-Induced Skin Damage Mitigation

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The rats’ dorsal sides were shaved 24 h before starting the experiment. Thirty rats were randomly allocated into five groups, each containing 6 animals (n = 6). Gp I: normal control group; rats were not exposed to any irradiation and did not receive any treatment, Gp II: UVB group; rats were exposed to UVB-irradiation and did not receive any treatment, Gp III: positive standard group (Vitamin A palmitate), Gp IV: FO group and Gp V: FO-SLNs group. Groups III, IV and V were UVB-irradiated and respectively received Vitamin A palmitate, FO and FO-SLNs. A UV lighter (peak emission was 302 nm, CL-1000 M, UVP, Upland, CA, USA) was used for UVB irradiation. UVB irradiation doses were 40–80 mJ/cm2 (exposure time was 15–30 s) and the lamp was fixed 5 cm above the platform where rats were placed [52 (link)]. Rats received topical treatments once daily on dorsal surfaces, prophylactically 2 h before the UVB exposure for ten consecutive days.
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9

UV-Induced Skin Damage and K36H Treatment

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Six-week-old female BALB/c hairless mice were randomly divided into the following five groups (six per group): control group, UVB-irradiated group, UVB-irradiated and vehicle-treated group, UVB-irradiated and 25-μM-K36H-treated group, and UVB-irradiated and 100-μM-K36H-treated group. Mice were exposed to UVB irradiation (302 nm UV, 5 × 8 watt UV dual bipin discharge type, CL-1000M, UVP, Upland, CA, USA) three times per week and were treated with 50 μL of vehicle (glycerol) or K36H (25 or 100 μM) every day for 12 weeks, as previously described [42 (link)]. The UVB dose was 36 mJ/cm2 in the first week, 54 mJ/cm2 in the 2–4 weeks, 72 mJ/cm2 5–7 weeks, and 108 mJ/cm2 8–10 weeks [42 (link)].
Erythema and transepidermal water loss (TEWL) were measured using an MPA 580 system (Courage + Khazaka electronic GmbH, Cologne, Germany) [28 (link)].
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10

Photoaging Models: UVB and UVA Protocols

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The UVB and UVA photoaging models were established based on the experimental protocol of Wu and Lan [3 (link),43 (link)]. For UVB radiation, UV light (broadband with peak emission at 302 nm, CL-1000 M (Analytik Jena US LLC, formerly UVP, California, Upland, CA 91786, USA) was used. UVB-irradiated mice were exposed to a gradually increasing dose of UVB irradiation thrice a week: first week, 36 mJ/cm2; second to fourth week, 54 mJ/cm2; fifth to the seventh week, 72 mJ/cm2; and eighth to the tenth week, 108 mJ/cm2 [3 (link)].
UVA-irradiated mice received energy of 8 J/cm2, three times a week for 8 weeks with CL1000 L UVA light (UVP, Upland, USA; emission spectrum 320–400 nm with a peak wavelength at 365 nm) [43 (link)].
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