Ns

Note

Values summarize data from Figure 1 in Strickland etal. (1994). NS is not significantly different, indicates that no significant immune suppression is occurring. It should be noted that in the legend to that Figure 1, there is a printer's error and the amount of challenging FITC is given as 10 ml rather than 10 jll.

Note

Values summarize data from Figure 1 in Strickland etal. (1994). NS is not significantly different, indicates that no significant immune suppression is occurring. It should be noted that in the legend to that Figure 1, there is a printer's error and the amount of challenging FITC is given as 10 ml rather than 10 jll.

Table 12.5 Crude A. barbadensis ARF Process A gel protects the local cutaneous hypersensitivity immune response from low dose (2,000 Joules/m2) UV radiation.

Percentage decrease from homologous control (Groups of 15 mice each)

No Treatment Vehicle 0.5% Aloe

p versus homologous control <0.001 <0.001 NS

Note

Values summarize data from Figure 4 in Strickland etal. (1994). NS is non-significant, indicating that no significant immune suppression is occurring. The experiment was performed on groups of five mice each and was repeated three times. Analysis of variance revealed that with three repeats, experiment to experiment variability was non-significant.

controls (UVB, ~4—5mmX 10-2 ear swelling versus ~9-10mmX10-2 in unirradiated controls). Treatment with aloe after UVB injury almost completely prevented the UVB-induced suppression of CHS induction. Swelling was ~8mm X10-2, 87 to 91% of that usually observed.

The amount of daily UV radiation, 400 Joules/m2, in the experiment above is quite small, not quite the minimal erythemal dose (MED) for the C3H mouse. We therefore also tested the protective ability of crude aloe materials at a dose (2,000Joules/m2) just sufficient to cause a minimal sunburn (Table 12.5 above).

The effect is essentially identical to that described in Table 12.4. UV radiation decreases the T cell-mediated CHS response by about one half. Treatment of the skin with ARF Process A gel immediately after injury restores the immune response to where there is no longer statistically significant suppression by UV. Interestingly, we almost never observe a protective effect where the UV versus UV + aloe values are numerically identical, even through there is not a statistical difference between them.

Recently, our findings with crude materials have been verified by other investigators (Lee, 1999). Aloe's ability to prevent some of the consequences of UV-induced injury make it a potentially useful adjunct to sunscreens.

Effects of A. barbadensis gel on suppression of cutaneous hypersensitivity — local versus systemic actions

Aloe, applied topically, may act locally by penetrating the epidermis and preventing immunosuppression or it may penetrate and have a systematic action. To distinguish between these two possibilities the abdominal skin of mice was treated with a single 2,000Joules/m2 dose of UVB. Various sites, non-irradiated back versus irradiated abdomen, were then treated with vehicle or 0.5% ARF Process A gel. Three days after injury and treatment, the mice were immunized on the abdominal skin with FITC. One week later their sensitization status was determined via challenge on the ear. Table 12.6 gives the results.

Aloe gel protected the CHS response from UV suppression only when it was applied to the injured skin. This finding indicates that although the gel is being absorbed

Table 12.6 Crude A. barbadensis ARF Process A gel protects the cutaneous hypersensitivity immune response from low dose (2,000 Joules/m2) UV radiation only when the site of injury is treated.

Percentage decrease from homologous control (Groups of five mice each)

NoTreatment Vehicle to 0.5% Aloe 0.5% Aloe abdomen to abdomen to back

2000 Joules/m2 to abdominal 59% 53% 29% 55%

skin

Note

Values summarize data from Table IV in Strickland etal. (1994). Significance of site to site treatment effect, back versus abdomen, p = 0.03.

Table 12.7 Crude A. barbadensis ARF Process A gel prevents systemic suppression of the cutaneous hypersensitivity immune response by high dose (10,000 Joules/m ) UV radiation.

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