Antioxidant axis Nrf2-keap1-ARE in inhibition of alcoholic liver fibrosis by IL-22

Table 1 Effects of acetaldehyde on hepatic stellate cells-T6 cell proliferation for 24 h and 48 h, and maximum OD value after exposure to 200 μmol/L acetaldehyde

Concentration ofacetaldehyde (μmol/L)	24 h		48 h
	OD	Proliferation rate	OD	Proliferation rate
0	0.2743 ± 0.0134		0.4154 ± 0.0130
25	0.3409 ± 0.0118a	124%	0.4983 ± 0.0258a	120%
50	0.3732 ± 0.0152a	136%	0.5733 ± 0.0208a	138%
100	0.3807 ± 0.0157a	139%	0.6181 ± 0.0351a	149%
200	0.5019 ± 0.0098a	183%	0.7649 ± 0.0333a	184%
400	0.4524 ± 0.0104a	165%	0.7069 ± 0.0265a	170%

Data are expressed as mean ± SD.

^aP < 0.05 vs the control group.

Table 2 Effects of interleukin-22 on the acetaldehyde-induced HSC-T6 cells proliferation

Group	OD	Proliferation inhibition rate
Control group	0.3854 ± 0.0366
Model group	0.7860 ± 0.0129a	-
10 ng/mL IL-22 group	0.6761 ± 0.0129ac	14%
20 ng/mL IL-22 group	0.5903 ± 0.0164ac	25%
50 ng/mL IL-22 group	0.5095 ± 0.0101ac	35%

OD was significantly decreased along with increased IL-22 dose, indicating that IL-22 dose-dependently inhibited proliferation of HSCs. Data are expressed as mean ± SD.

^aP < 0.05 vs the control group;

^cP < 0.05 vs the model group. HSCs: Hepatic stellate cells; IL: Interleukin.

Table 3 Content of malondialdehyde and glutathione in the supernatant

Group	Acetaldehyde (μmol/L)	IL-22 (ng/mL)	MDA (nmol/mL)	GSH (NU/L)
Control group	0	0	1.3654 ± 0.1022	12.8569 ± 0.3699
Model group	200	0	7.5073 ± 0.6126a	24.6972 ± 0.5043a
IL-22 groups
Low	200	10	5.1256 ± 0.3835ac	33.8866 ± 2.6506ac
Medium	200	20	3.3195 ± 0.2963ac	44.5935 ± 4.1386ac
High	200	50	2.8141 ± 0.0720ac	55.6834 ± 1.1671ac

Data are expressed as mean ± SD.

^aP < 0.05 vs the control group;

^cP < 0.05 vs the model group. GSH: Glutathione; MDA: Malondialdehyde; IL: Interleukin.