Moringa oleifera have laxative effects, but their active compositions and mechanisms are not very clear thus far. To this end, we systematically explored the active components and mechanism of M. oleifera leaves in relieving constipation by using the slow transit constipation (STC) mouse model and network pharmacology. The results of animal experiments showed that M. oleifera aqueous extract (MOA) had good laxative activity, and its 70% alcohol soluble part (ASP) also showed significant laxative activity (P < 0.01). Network pharmacological prediction results suggested that L-phenylalanine (Phe) was the key compound of ASP, and it might relieve constipation through tachykinin receptor 1 (TACR1) and three kinds of adrenergic receptors, including α1A (ADRA1A), α2A (ADRA2A), and α2B (ADRA2B). Further animal experiment results showed that Phe significantly promoted gastrointestinal motility. Phe may relieve STC by enhancing the release of substance P (SP) and upregulating the mRNA expression of TACR1 in the ileum. Importantly, Phe may also promote intestinal movement by downregulating the mRNA expression of ADRA2A and ADRA2B and upregulating the mRNA expression of Calm and the mRNA and protein expression of myosin light chain 9 in the ileum, thereby activating the G protein-coupled receptor-myosin light chain signaling pathway. These results lay a foundation for the application of M. oleifera and Phe in constipation.


Amomum tsaoko is an important food and medicinal plant. Its dried fruit is rich in alkaloids and is known to have a notable laxative effect. Nevertheless, it remains unclear whether alkaloids from A. tsaoko can relieve constipation. The present study sought to purify alkaloids from A. tsaoko via the macroporous resins method and to investigate the laxative activity of alkaloid-rich A. tsaoko extract (ARAE). HP-20 was identified as the most efficient resin for purifying alkaloids from A. tsaoko. ARAE was predominantly concentrated in indole-3-carboxaldehyde, p-octopamine, phyllalbine, synephrine, lumichrome, and isatidine. The results of animal experiments demonstrated that ARAE markedly promoted gastrointestinal motility and shortened the defecation time of mice with functional constipation (FC). ARAE not only significantly affected the serum level of AChE but also upregulated the expression of 5-HT4R, c-Kit, SCF and smMLCK as well as the protein expression of c-Kit in the colon. Furthermore, ARAE increased the number of goblet cells in the colon, facilitated the secretion of acidic mucus, and increased the expression of intestinal barrier factors. Importantly, ARAE had a considerable influence on the structure and composition of the gut microbiota in mice with FC. The correlation analysis results suggested that ARAE may facilitate intestinal microecological balance by regulating key microbial populations, including Lachnospiraceae_NK4A136_group, Rikenellaceae_RC9_gut_group, norank_f_Desulfovibrionaceae, norank_o_Clostridia_vadinBB60_group, and Faecalibaculum. ARAE can alleviate FC by regulating gastrointestinal motility and the intestinal microecosystem. The potential applications of A. tsaoko and ARAE in the development of laxative health foods and pharmaceuticals are significant and warrant further investigation.

Some visitors to India often experience diarrhea and attribute it to Indian food; however, murine food allergy model have shown that diarrhea occurring after consumption of Moringa may be due to an allergic reaction. The findings of this study indicate that Moringa leaf protein (Mo-Pr)1 has the potential to sensitize BALB/c mice. Mo-Pr has been demonstrated to stimulate the mice's production of Mo-Pr-specific IgE, promote mast cell degranulation, and induce the release of histamine and other inflammatory mediators. Mo-Pr has been demonstrated to promote the proliferation and differentiation of Th2 cells while simultaneously inhibiting the proliferation and differentiation of Th1 and Treg cells. The sera western blot shown that the significant band Mo-Pr molecule weight is 36 kDa respectively, which was identified as fructose-1,6-bisphosphate aldolase (FBA) by LC-MS\MS.