Magnoflorine (Mag) has multiple pharmacological activities for the prevention and treatment of prostatitis. However, its molecular mechanisms andpharmacological targets are not clear. In this study, the ultra-performance liquid tandem mass spectrometry-based metabolomics method was used to clarify the intervention of Mag against prostatitis and the biological mechanism. A total of 25 biomarkers associated with the prostatitis model were identified by metabolomics, and a number of metabolic pathways closely related to the model were obtained by MetPA analysis. After given Mag treatment, the results of each indicator were shown that Mag alkaloid could inhibit the development of prostatitis effectively. We found that Mag had regulative effects on potential biomarkers of prostatitis model, which can regulate them to the control group. Our results indicated that alkaloids have an effective intervention therapy for prostatitis, and five types of metabolic pathways closely related to prostatitis model were obtained, including phenylalanine, tyrosine and tryptophan biosynthesis, phenylalanine metabolism, tyrosine metabolism, arginine and proline metabolism, glycine, serine and threonine metabolism, alanine, aspartate and glutamate metabolism. This study has provided the basic experimental data for the development of Mag in the prevention and treatment of prostatitis.
Glaucoma is a severe blindness‐causing optic nerve disease characterized by a loss of retinal ganglion cells (RGCs). Previous studies have shown that the Tongqiao Mingmu (TQMM) formula can reduce retinal and optic nerve damage, but its mechanism of action requires further elucidation. In this study, an RGC injury model was prepared using glutamate and then treated with serum‐containing drug from the TQMM formula (hereafter called “TQMM formula serum”). In the glutamate‐induced RGC injury model, cell viability decreased with an increase in glutamate concentration, whereas the expression of autophagy‐related biomarkers LC3 and Belicin‐1 increased. An adenovirus transfection experiment revealed that glutamate markedly promoted autophagic flux in RGCs. Notably, TQMM formula serum inhibited the expression of autophagy‐related biomarkers, reduced autophagy flux, and reversed the damage caused by glutamate to RGCs. Furthermore, the PI3K inhibitor LY294002 was used to intervene in the RGC autophagy model and was found to suppress the PI3K/AKT/mTOR pathway and enhance RGC autophagy. However, TQMM formula serum could generate an opposite effect and upregulate the expressions of the PI3K/AKT/mTOR pathway genes and proteins. In conclusion, the TQMM formula can prevent glutamate‐induced autophagy in RGCs, possibly by activating the PI3K/AKT/mTOR pathway and reducing the expression of autophagy‐related biomarkers LC3 and Belicin‐1 to attenuate autophagy and maintain RGC viability.
A Corrigendum on Liquid chromatograph-mass spectrometry-based non-targeted metabolomics discovery of potential endogenous biomarkers associated with prostatitis rats to reveal the effects of magnoflorine
Streptozotocin (STZ)-induced diabetes mellitus (DM) model shows the signal of cardiac dysfunction,
which is manifested as myocardial fibrosis and hypertrophy. This study was designed to predict targets
of sodium hydrosulfide (NaHS) for diabetic cardiomyopathy and its corresponding triggered pathways
by network pharmacology analysis and test the effects of NaHS as well as its mechanism as possible
modulators of left ventricular remodeling in diabetic rats. The drug-target networks were constructed via
approaches of network pharmacology, and the predicted targets and pathways were validated by in vivo
experiments. Rats were randomly divided into 3 groups (n=6/group): STZ-induced DM group (STZDM); STZ-induced DM treated with H2S group (STZ-NaHS); control group. The control group was
treated with daily saline (i.p.); the diabetic model was induced by intraperitoneal (i.p.) injections of 40
mg/kg/day STZ. After 12 weeks, the rat cardiac function was determined, and the pathological
morphology of the heart was analysed by Masson trichrome staining in each group. The expression level
of matrix metalloproteinase 9 (AGEs), CSE, CBS and several autophagy associated proteins were
detected by the ELISA analysis. Results from the PPI network implied that 27 targets were key regulators.
The AGE-RAGE signaling pathway in diabetic complications and the apoptotic signaling pathway was
discovered to be the key to anti-diabetic cardiomyopathy of NaHS upon the GO enrichment analyses and
KEGG pathway. In the in vivo experiment, compared with the control group, cardiac fibrosis and
attenuated left ventricular function were observed. Furthermore, compared with the control group, the
expression level of CSE, CBS and autophagy associated proteins Atg5 was significantly decreased, while
that of AGEs, autophagy associated proteins p62 and p-ERK1/2 was significantly increased in the STZDM group (P<0.05). In the STZ-NaHS group, cardiac fibrosis and ventricular dysfunction were
ameliorated, the expression level of CSE, CBS and autophagy associated proteins Atg5 was increased,
and the expression level of AGEs, autophagy associated proteins p62 and p-ERK1/2 was significantly
decreased (P<0.05). In conclusion, H2S may alleviate cardiac fibrosis of the STZ-induced DM rat model
by enhancing cardiac autophagy, inhibiting cardiomyocyte apoptosis and downregulating p-ERK1/2.
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