## 4 Discussion
SS can inhibit the release of gastrointestinal hormones, slow down gastric emptying, and reduce smooth muscle contraction, which might cause constipation [26]. VIP is an inhibitory neurotransmitter that stimulates peristalsis and promotes gastrointestinal motility [27]. The SS level was highest in the model group, while it was significantly decreased in the LP-CQPC10 group (\(p<0.05\)), suggesting that LP-CQPC10 could have a preventive effect on constipation. In the metabolism, superoxide anions (O\({}_{2}\)\({}^{-}\)) and oxygen radicals participate in physiological reactions in the body. Imbalance will greatly increase O\({}_{2}\)\({}^{-}\) and oxygen radicals, which will disorder the metabolism [28]. It has been reported that the Cu/Zn-SOD activity in patients with constipation is lower than in normal people. The likely reason is that long-term retention and stimulation of hard faeces causes inflammation in the intestinal tract [29]. Mn-SOD can reduce the activity under inflammation [30]. SOD can transform harmful superoxide radicals into hydrogen peroxide. Although hydrogen peroxide is still harmful to the body, CAT can degrade it into water. SOD and CAT will form into an oxidation resistant chain to remit the damage to the intestinal tract that is caused by constipation [31]. The results of our study indicate that LP-CQPC10 could effectively remit the reduced activity of Cu/Zn-SOD, Mn-SOD, and CAT caused by constipation. Cajal cells (ICC) are a type of special mesenchymal cells. Colon ICC amount, morphological change, and abnormality of the cellular network structure will slow the peristalsis rate, further leading to slow transit constipation [32]. C-Kit is one of the specific markers for ICC, and SCF is the natural ligand of the C-kit receptor [33]. It has been reported that ICC density in the small intestine of patients with constipation is decreased, indicating that reduced ICC is related to the down-regulation of the c-Kit gene in the sigmoid colon, and reduced c-kit protein and mRNA expression [34]. The results showed that the mRNA expression of both c-Kit and SCF in the LP-CQPC10 group was significantly increased (\(p<0.05\)), suggesting that LP-CQPC10 could increase the ICC amount and thus remit constipation. TRPV1 is closely related to defecation and activation of TRPV1 could trigger the release of neurotransmitters, thus leading to intestinal motility dysfunction. The increase in TRPV1 expression is an important manifestation of intestinal injury and the damage that is caused by gastrointestinal tract diseases can increase TRPV1 expression in patients with constipation [35]. GDNF regulates ganglion cells and aids the repair of the damaged intestinal tract, while also preventing constipation. Constipation is related to the intestinal nervous system, leading to muscular tension and weak gastrointestinal motility [36]. Regulation of TRPV1 and GDNF expression is one of the important mechanisms to remit constipation. LP-CQPC10 also exerts such an effect of constipation remission. NOS participates in the regulation of gastrointestinal motility. An increase in NOS will lead to an increase in the NO content, influencing intestinal function and leading to constipation [37]. Continuous increase of NO can cause a more severe colonic motility disorder [38]. Endothelial dysfunction can cause constipation and the decrease in NO bioavailability is an important factor for this dysfunction [39]. NO is synthesized via NOS catalysis. Three subtypes for NOS have been described, including NOS1 (nNOS), NOS2 (iNOS), and NOS3 (eNOS) [40]. Under normal physiological conditions, NO in vascular endothelial cells mainly originates from eNOS, whose main effect is the regulation of the normal physiological function [41]. The expression of nNOS is greatly decreased in the small intestine of animals with constipation [42]. iNOS is not expressed under the resting-state, while a high level of iNOS and NO will be generated when the body is injured or under other pathological conditions [43].