Investigation of the Repairing Effect and Mechanism of Oral Degraded Sericin on Liver Injury in Type II Diabetic Rats

Abstract

In the sericulture and silk production industry, sericin is discharged in the degumming wastewater, resulting in a large amount of wasted natural protein and environmental pollution. This study investigated the effect of degraded sericin recovered by the Ca(OH)₂-ultrasound degumming method (a green process) on liver injury in T2D rats. After 4 weeks of dietary sericin supplementation, the liver masses and organ coefficients of the T2D rats improved compared with those of the model rats that were not fed sericin. Oral sericin activated the damaged PI3K/AKT/AMPK pathway to enhance glycogen synthesis, accelerate glycolysis, and inhibit gluconeogenesis. The protein expression levels of the inflammatory factors NF-κB, IL-6, and TNF-α in the T2D model group were up to two times higher than in the normal group. However, all three T2D groups that received oral sericin showed significant decreases in these factors to the level found in the normal group, indicating that inflammation in the body was significantly reduced. These results show that the sericin protein might improve glycogen synthesis, accelerate glycolysis, and inhibit gluconeogenesis by enhancing the anti-oxidation capability and reducing inflammatory reactions. Therefore, sericin recovered by Ca(OH)₂ degradation has potential use in the development of functional health foods that can lower blood sugar.

Keywords: inflammatory factors; oral administration; protein expression; sericin; signaling pathway.

Figure 1

Effect of oral sericin on the expression of key hepatic glucose metabolism proteins in T2D rats. Normal: normal group; Model: diabetic model group; PC: 0.5% melbin; LLS, MLS, and HLS: 1%, 2.5%, and 5% LS, respectively. n = 3, ** p < 0.01 versus normal group. ^# p < 0.05, ^## p < 0.01 versus model group.

Figure 2

Effect of oral sericin on the expression of PI3K/AKT pathway proteins in T2D rats. Normal: normal group; Model: diabetic model group; PC: 0.5% melbin; LLS, MLS, and HLS: 1%, 2.5%, and 5% LS. n = 3, ^# p < 0.05, ^## p < 0.01 versus model group.

Figure 3

Effect of sericin on the expression of key AMPK/ACC proteins in T2D rats. Normal: normal group; Model: diabetic model group; PC: 0.5% melbin; LLS, MLS, and HLS: 1%, 2.5%, and 5% LS. n = 3, ^# p < 0.05, ^## p < 0.01 versus model group.

Figure 4

Effect of oral sericin on TNF-α, IL-6, and NF-κB levels in livers of T2D rats. (a–c) are TNF-α, IL-6, and NF-κB levels, respectively. Normal: normal group; Model: diabetic model group; PC: 0.5% melbin administration; LLS, MLS, and HLS: 1%, 2.5%, and 5% L. n = 3, ** p < 0.01 versus normal group. ^## p < 0.01 versus model group.

Figure 5

Possible pathways through which oral sericin might affect T2D rats. ↓ & ↑, means upstream and downstream of the pathway and feedback regulation, respectively.