Abstract
Objectives. The Chinese herbal medicine Da-Cheng-Qi Decoction (DCQD) can ameliorate the severity of acute pancreatitis (AP). However, the potential pharmacological mechanism remains unclear. This study explored the potential effective components and the pharmacokinetic characteristics of DCQD in target tissue in experimental acute pancreatitis in rats. Methods. Acute pancreatitis-like symptoms were first induced in rats and then they were given different doses of DCQD (6 g/kg, 12 g/kg, and 24 g/kg body weight) orally. Tissue drug concentration, tissue pathological score, and inflammatory mediators in pancreas, intestine, and lung tissues of rats were examined after 24 hours, respectively. Results. Major components of DCQD could be found in target tissues and their concentrations increased in conjunction with the intake dose of DCQD. The high-dose compounds showed maximal effect on altering levels of anti-inflammatory (interleukin-4 and interleukin-10) and proinflammatory markers (tumor necrosis factor α and interleukin-6) and ameliorating the pathological damage in target tissues (P < 0.05). Conclusions. DCQD could alleviate pancreatic, intestinal, and lung injury by altering levels of inflammatory cytokines in AP rats with tissue distribution of its components.
Highlights
Acute pancreatitis (AP) is an acute inflammation of the pancreas and surrounding tissue caused by pancreatic digestive enzymes
The rats treated with Da-Cheng-Qi Decoction (DCQD) had a significant reduction of inflammatory cell infiltration, hemorrhaging, necrosis, and interstitial edema compared to model group (MG), the greatest effect being seen in the high-dose treatment group (HDG)
DCQD reduced the standard pathological scores of the pancreas affected by experimental AP, and the scores of median-dose treatment group (MDG) and HDG were significantly lower than that in the MG at 24 hours (Figures 1(a1) and 1(a2))
Summary
Acute pancreatitis (AP) is an acute inflammation of the pancreas and surrounding tissue caused by pancreatic digestive enzymes. Usually self-limiting, up to 20% of patients develop a severe form of disease, which can lead to a systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction and failure [1]. Intestinal injury caused by AP is closely associated with poor prognosis in severe AP patients and is believed to be the primary cause of acute lung injury progression [7,8,9,10]. The adjuvant use of herbal medicine and electroacupuncture ameliorated lung and intestinal injury and led to a marked reduction in morbidity and mortality in China [11,12,13,14]. Recent studies have shown that DCQD can promote gastrointestinal motility, reduce acute lung injury, and inhibit cytokine activity and inflammatory responses in AP [15,16,17,18]. The pharmacological characteristics and bioactivities of DCQD inside the target tissue of AP rats are still not clear, even though there has been some progress in serum pharmacology [19, 22,23,24]
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