The effects of camel milk in systemic inflammation and oxidative stress of cigarette smoke-induced chronic obstructive pulmonary disease model in rat

Abstract

Background: The effects of camel milk in inflammation and systemic oxidative stress of cigarette smoke (CS)-induced chronic obstructive pulmonary disease (COPD) associated with small airway inflammation in rats were investigated.

Methods: 35 male Wistar rats were randomly divided into five groups: (a) control, (b) CS-exposed rats, c and (d) CS-exposed rats treated with the 4 and 8 mL/kg camel milk, and (e) CS-exposed rats treated with 1 mg/kg dexamethasone.

Results: Total and differential WBC counts, serum level of TNF-α and malondialdehyde (MDA) level in serum and homogenized tissues of the heart, kidney, liver, and testicle were significantly increased, but catalase (CAT), superoxide dismutase (SOD) and thiol levels were significantly decreased in CS-exposed rats (p < 0.01 to p < 0.001). Treatment with dexamethasone and both doses of camel milk improved all measured variables compared to the COPD group (p < 0.05 to p < 0.001). The improvements of most variables in the treated group with high dose of camel milk were higher than the effect of dexamethasone (p < 0.05 to p < 0.001). These findings suggest that camel milk has a therapeutic potential for treating systemic oxidative stress and inflammatory induced by CS.

Conclusion: Therefore, camel milk might be effective in attenuating the effects of CS-induced systemic inflammation and oxidative stress.

Keywords: COPD; camel milk; cytokine; oxidative stress; pulmonary disease.

Figure 1

Flowchart of the study design of the animal model.

Figure 2

Effects of camel milk on improving total and differential WBC counts in the blood of CS-exposed rats. Data are presented as mean ± SEM (n = 7 in each group). *p < 0.05, **p < 0.01 and ***p < 0.001; compared to the control group. +p < 0.05, ++p < 0.01 and +++p < 0.001; compared to untreated COPD group. £p < 0.05 and ££p < 0.01; compared to COPD group-treated with 4 mL/kg camel milk. ##p < 0.01 and ###p < 0.001; compared to Dexa group. ANOVA and Tukey–Kramer test were used for statistical analysis.

Figure 3

Effect of camel milk on improving TNF-α level in serum of CS-exposed rats. Data are presented as mean ± SEM (n = 7 in each group). **p < 0.01 and ***p < 0.001; compared to the control group. ++p < 0.01 and +++p < 0.001; compared to untreated COPD group. £p < 0.05; compared to COPD group-treated with 4 mL/kg camel milk. #p < 0.05 and ###p < 0.001; compared to Dexa group. ANOVA and Tukey–Kramer test were used for statistical analysis.

Figure 4

Effects of camel milk on improving CAT, SOD, thiol and MDA levels in serum of CS-exposed rats. Data are presented as mean ± SEM (n = 7 in each group). *p < 0.05, **p < 0.01 and ***p < 0.001; compared to the control group. ++p < 0.01 and +++p < 0.001; compared to untreated COPD group. £p < 0.05, ££p < 0.01 and £££p < 0.001; compared to COPD group-treated with 4 mL/kg camel milk. #p < 0.05 and ##p < 0.01; compared to Dexa group. ANOVA and Tukey–Kramer test were used for statistical analysis.

Figure 5

Effects of camel milk on improving SOD levels in the heart (A), kidney (B), liver (C), and testicle tissues (D) of CS-exposed rats. Data are presented as mean ± SEM (n = 7 in each group). *p < 0.05, **p < 0.01 and ***p < 0.001; compared to the control group. +p < 0.05, ++p < 0.01 and +++p < 0.001; compared to untreated COPD group. ££p < 0.01 and £££p < 0.001; compared to COPD group-treated with 4 mL/kg camel milk. #p < 0.05, ##p < 0.01 and ###p < 0.001; compared to Dexa group. ANOVA and Tukey–Kramer test were used for statistical analysis.

Figure 6

Effects of camel milk on improving CAT levels in the heart (A), kidney (B), liver (C), and testicle (D) tissues of CS-exposed rats. Data are presented as mean ± SEM (n = 7 in each group). **p < 0.01 and ***p < 0.001; compared to the control group. +p < 0.05, ++p < 0.01 and +++p < 0.001; compared to untreated COPD group. £p < 0.05 and ££p < 0.01; compared to COPD group-treated with 4 mL/kg camel milk. #p < 0.05, ##p < 0.01 and ###p < 0.001; compared to Dexa group. ANOVA and Tukey–Kramer test were used for statistical analysis.

Figure 7

Effects of camel milk on improving thiol levels in the heart (A), kidney (B), liver (C), and testicle (D) tissues of CS-exposed rats. Data are presented as mean ± SEM (n = 7 in each group). **p < 0.01 and ***p < 0.001; compared to the control group. +p < 0.05, ++p < 0.01 and +++p < 0.001; compared to untreated COPD group. £p < 0.05 and ££p < 0.01; compared to COPD group-treated with 4 mL/kg camel milk. #p < 0.05 and ##p < 0.01; compared to Dexa group. ANOVA and Tukey–Kramer test were used for statistical analysis.

Figure 8

Effects of camel milk on improving MDA levels in the heart (A), kidney (B), liver (C), and testicle (D) tissues of CS-exposed rats. Data are presented as mean ± SEM (n = 7 in each group). ***p < 0.001; compared to the control group. +p < 0.05, ++p < 0.01 and +++p < 0.001; compared to untreated COPD group. £p < 0.05, ££p < 0.01 and £££p < 0.001; compared to COPD group-treated with 4 mL/kg camel milk. #p < 0.05 and ###p < 0.001; compared to Dexa group. ANOVA and Tukey–Kramer test were used for statistical analysis.