Objective: To investigate the effects of berberine(BBR) and cinnamic acid(CA), the main active components in Jiaotai Pill(交泰丸, JTP), on palmitic acid(PA)-induced intracellular triglyceride(TG) accumulation in NIT-1 pancreatic β cells. Methods: Cells were incubated in culture medium containing PA(0.25 mmol/L) for 24 h. Then treatments with BBR(10 μmol/L), CA(100 μmol/L) and the combination of BBR and CA(BBR+CA) were performed respectively. Intracellular lipid accumulation was assessed by Oil Red O staining and TG content was measured by colorimetric assay. The expression of adenosine monophosphate-activated protein kinase(AMPK) protein and its downstream lipogenic and fatty acid oxidation genes, including fatty acid synthase(FAS), acetyl-co A carboxylase(ACC), phosphorylation acetyl-co A carboxylase(p ACC), carnitine acyl transferase 1(CPT-1) and sterol regulating element binding protein 1c(SREBP-1c) were determined by Western blot or real time polymerase chain reaction. Results: PA induced an obvious lipid accumulation and a significant increase in intracellular TG content in NIT-1 cells. PA also induced a remarkable decrease in AMPK protein expression and its downstream targets such as p ACC and CPT-1. Meanwhile, AMPK downstream lipogenic genes including SREBP-1c m RNA, FAS and ACC protein expressions were increased. Treatments with BBR and BBR+CA, superior to CA, significantly reversed the above genes changes in NIT-1 pancreatic β cells. However, the synergistic effect of BBR and CA on intracellular TG content was not observed in the present study. Conclusion: It can be concluded that in vitro, BBR and BBR+CA could inhibit PA-induced lipid accumulation by decreasing lipogenesis and increasing lipid oxidation in NIT-1 pancreatic β cells.
Objective: To explore the effect and mechanism of Jiaotai Pill(交泰丸, JTW) on intestinal mucosal damage in rats with chronic partial sleep deprivation(PSD). Methods: Obesity resistant(OR) rats were selected, and underwent 4 h PSD by being exposed to environmental noise for 4 weeks. During the whole PSD period, JTW and estazolam were orally given to the rats respectively in the treating groups. Plasma concentration of lipopolysaccharide(LPS) which is the marker of gut-origin endotoxemia was examined. Intestinal morphology changes were observed by optical microscopy. The protein expression of occludin(Ocln) in the intestine was measured by immunofluorescence technique and Western blot. The expressions of circadian proteins cryptochromes(Cry1 and Cry2) in the intestine were also determined. Results: The treatment of JTW significantly decreased LPS level in OR rats with PSD(P<0.05). JTW also attenuated insomnia-induced intestinal injury like shorter, sparse and incomplete villus, wide gap between the villus, mucosal swelling and congesting(P<0.05). These changes were associated with the effect of JTW on up-regulating the expressions of Cry1 protein, Cry2 protein and Ocln protein in the intestine. Conclusions: JTW has the beneficial effect on improving intestinal mucosal damage caused by PSD. The mechanism appears to be related to the modulation of the expressions of circadian proteins and Ocln protein in the intestine, thereby attenuating inflammation and improving insulin resistance in insomnia rats.
