Psychoactive Plant Database - Neuroactive Phytochemical Collection

1. Transl Androl Urol. 2024 Oct 31;13(10):2209-2228. doi: 10.21037/tau-24-274.
Epub  2024 Oct 28.

Comparison of different processed products of Allium tuberosum Rottler for the 
treatment of mice asthenozoospermia.

Wu W(#)(1), Guo X(#)(1), Li J(1), Yang M(1), Xiong Y(2).

Author information:
(1)Institute of Chinese Pharmaceutical Preparations, Chongqing Traditional 
Chinese Medicine Hospital, Chongqing, China.
(2)Key Laboratory of Basic Pharmacology of Guizhou Province and School of 
Pharmacy, Zunyi Medical University, Zunyi, China.
(#)Contributed equally

BACKGROUND: Allium tuberosum Rottler improves sexual function and is used in the 
treatment of impotence and spermatorrhea. However, its chemical composition and 
mechanism of action remain unclear. This study investigates the chemical 
composition and mechanism of action of Allium tuberosum Rottler co-processed 
with salt and wine (GZP) in modulating testicular mitochondrial autophagy for 
the treatment of asthenozoospermia in mice.
METHODS: Adenine gavage + cyclophosphamide intraperitoneal injection was used to 
establish the model of asthenozoospermia, and six Allium tuberosum Rottler 
processed products were compared in the pharmacological efficacy for the 
treatment of asthenozoospermia in mice. The liquid chromatograph mass 
spectrometer (LC-MS) assay was performed to analyse the compositional changes in 
the GZP. The mechanism of GZP in the treatment of asthenozoospermia in mice was 
further investigated. The mitophagy was detected by transmission electron 
microscope (TEM) and immunofluorescence, respectively. Reactive oxygen species 
(ROS) were detected by probe. Protein expression was determined by Western 
blotting.
RESULTS: GZP exhibited optimal therapeutic effects on asthenozoospermia in mice. 
It showed the best therapeutic effect in improving the total number of 
spermatozoa, sperm survival rate, improving sperm viability and reducing sperm 
deformity rate, alleviating the abnormal pathological morphology of mice testis, 
and increasing the serum testosterone (T), follicle-stimulating hormone (FSH) 
and prolactin (PRL) levels in mice. The LC-MS detection found that Allicin 
showed the most significant increase in GZP. Besides, GZP reduced ROS level and 
inhibited mitophagy in mice testicular tissues. Meanwhile, it restrained the 
expression of PINK1, Parkin, Light chain 3II (LC3-II)/Light chain 3I (LC3-I) and 
Caspase-3 proteins.
CONCLUSIONS: GZP improves asthenozoospermia via inhibiting excessive mitophagy 
and protects the integrity of mitochondria by blocking the PINK1/Parkin 
signaling pathway. During which, the Allicin may play an important role.

2024 AME Publishing Company. All rights reserved.

DOI: 10.21037/tau-24-274
PMCID: PMC11535743
PMID: 39507862

Conflict of interest statement: Conflicts of Interest: All authors have 
completed the ICMJE uniform disclosure form (available at 
https://tau.amegroups.com/article/view/10.21037/tau-24-274/coif). The authors 
have no conflicts of interest to declare.


2. Vet World. 2024 Sep;17(9):2104-2114. doi: 10.14202/vetworld.2024.2104-2114.
Epub  2024 Sep 20.

House cricket protein hydrolysates alleviate hypertension, vascular dysfunction, 
and oxidative stress in nitric oxide-deficient hypertensive rats.

Sangartit W(1), Suwannachot P(2), Thawornchinsombut S(3), Jan-On G(4)(5), Boonla 
O(6), Senaphan K(2).

Author information:
(1)Department of Physiology, Faculty of Medicine, Khon Kaen University, Khon 
Kaen, 40002, Thailand.
(2)Division of Physiology, Faculty of Veterinary Medicine, Khon Kaen University, 
Khon Kaen, 40002, Thailand.
(3)Department of Food Technology, Faculty of Technology, Khon Kaen University, 
Khon Kaen, 40002, Thailand.
(4)Chulabhorn International College of Medicine, Thammasat University, 
Pathumthani, 12120, Thailand.
(5)Thammasat University Research Unit in Physiology and Integrated Medicine, 
Thammasat University, Pathumthani, 12120, Thailand.
(6)Department of Physical Therapy, Faculty of Allied Health Sciences, Burapha 
University, Chonburi, 20131, Thailand.

BACKGROUND AND AIM: Edible insects with high protein content and bioactive 
peptides with health promotion against chronic disease. Deficiency of nitric 
oxide (NO) contributes to hypertension, a leading cause of cardiovascular 
diseases and death worldwide. This study assessed the antihypertensive effects 
of house cricket protein hydrolysates (HCPH) in NO-deficient hypertensive rats.
MATERIALS AND METHODS: Male Sprague-Dawley rats (n = 12/group) were hypertensive 
after the administration of Nω-nitro-L-arginine methyl ester (L-NAME) at a dose 
of 50 mg/kg body weight (BW)/day in drinking water for 7 weeks. The animals were 
then treated with HCPH (250 or 500 mg/kg BW/day) or lisinopril (Lis) (1 mg/kg 
BW/day) for the last 4 weeks of L-NAME administration. Blood pressure (BP), 
vascular function, and structural changes, endothelial NO synthase (eNOS), and 
p47phox nicotinamide adenine dinucleotide phosphate (NADPH) oxidase protein 
expression in aortic tissues, plasma nitrate/nitrite, plasma 
angiotensin-converting enzyme (ACE) activity, and oxidative stress markers in 
blood and tissues were evaluated.
RESULTS: Induction of hypertension resulted in significantly elevated BP, 
decreased plasma nitrate/nitrite concentration, abolished vascular function, and 
increased vascular wall thickness. Overproduction of carotid and mesenteric 
superoxide, increased plasma, heart, and kidney malondialdehyde, and protein 
carbonyl levels, and increased plasma ACE activity were observed. 
Down-expression of eNOS with overexpression of p47phox NADPH oxidase subunit was 
also found in L-NAME hypertensive rats. Oral treatment with HCPH, particularly 
at a dose of 500 mg/kg BW/day, significantly alleviated these alterations in a 
manner comparable to that of Lis.
CONCLUSION: HCPH improved vascular function and exerted antihypertensive 
effects, mainly due to the improvement of NO bioavailability, reduction of 
oxidative stress, and inhibition of ACE.

Copyright: © Sangartit, et al.

DOI: 10.14202/vetworld.2024.2104-2114
PMCID: PMC11536747
PMID: 39507793

Conflict of interest statement: The authors declare that they have no competing 
interests.


3. J Microsc Ultrastruct. 2022 Aug 18;12(3):159-161. doi:
10.4103/jmau.jmau_17_21.  eCollection 2024 Jul-Sep.

Dapsone-induced Methemoglobinemia Case Report.

Islami MM(1).

Author information:
(1)Department of Pharmacy Practice, Faculty of Pharmacy, King Abdelaziz 
University, Jeddah, Saudi Arabia.

Methemoglobinemia is a rare disorder associated with an elevated methemoglobin 
level that occurs when hemoglobin is in the oxidized ferric ion form rather than 
reduced ferrous form. In patients with methemoglobinemia, the hemoglobin with 
oxidized ferric form cannot release oxygen to the tissues which leads to 
hypoxemia. Methemoglobinemia can be acquired or inherited. The acquired 
methemoglobinemia happens in patients after they take certain oxidizing drugs. 
This disorder is mostly treated with 2 mg/kg methylene. This disorder is mostly 
treated with 2 mg/kg methylene blue. However, administrating ascorbic acid as an 
antioxidant may also helpful, especially if a patient has taken two doses of 
methylene blue or if the use of methylene blue is contraindicated. 
Methemoglobinemia may not cure or may rebound after response to treatment, 
especially with long half-life drugs such as dapsone. As it states in the 
leaflet for methylene blue, if methemoglobinemia does not resolve after two 
doses, one should initiate another alternative. Ascorbic acid is a good 
alternative because it is an antioxidant to keep tissue from harm of free 
radicals and also has a role in reducing methemoglobin via co-factor 
nicotinamide adenine dinucleotide phosphate reeducates needed for glutathione 
metabolism. We discuss a case of methemoglobinemia treated successfully with 
oral ascorbic acid after using two doses of methylene blue. Oral ascorbic acid 
could be beneficial, especially when the patient was taken two doses of 
methylene blue.

Copyright: © 2022 Journal of Microscopy and Ultrastructure.

DOI: 10.4103/jmau.jmau_17_21
PMCID: PMC11537359
PMID: 39507646

Conflict of interest statement: There are no conflicts of interest.


4. Cureus. 2024 Oct 7;16(10):e70981. doi: 10.7759/cureus.70981. eCollection 2024 
Oct.

Benchmarking Point-of-Care Glucometers: A Comparative Study Using the Hexokinase 
Test and International Organization for Standardization (ISO) Standards.

George K(1), Joy S(2), Kaladi Palliyalil H(1), Shaji SM(1), Ajayakumar Sunanda 
V(1), Sreedevi A(1).

Author information:
(1)Community Medicine, Amrita Institute of Medical Sciences, Amrita Vishwa 
Vidyapeetham, Kochi, IND.
(2)Community Medicine, Amrita Institute of Medical sciences, Amrita Vishwa 
Vidyapeetham, Kochi, IND.

Introduction The International Diabetes Federation states that India accounts 
for one in seven of all adults with diabetes. Adherence to self-monitoring of 
blood glucose is essential for effective management of diabetes. Despite the 
wide variety of glucometers and their clinical applicability, there is a lot of 
ambiguity regarding their accuracy. Therefore, this study aimed to evaluate if 
three point-of-care glucometers using three different methods for the estimation 
of blood glucose fulfil the minimum accuracy needed by ISO15197:2013 when 
compared with the gold standard hexokinase test. Methods A cross-sectional study 
was conducted at two primary health care centers in Ernakulam district, which 
included 73 participants with diabetes and 73 without diabetes. We evaluated 
three different enzymes in the test glucometers: glucose dehydrogenase with 
pyrroloquinoline quinone (GDH-PQQ), glucose dehydrogenase with flavin adenine 
dinucleotide (GDH-FAD), and glucose oxidase (GOD). The glucometer readings were 
compared with the gold standard hexokinase test and ISO15197:2013 standards. To 
compare the accuracy of each glucometer with the reference method, the 
Bland-Altman plot was used and to evaluate the clinical significance of the 
differences between the glucometer and reference value the Clarke error grid 
analysis was performed. Results When compared with the gold standard hexokinase 
result, only 78.08% (GOD), 92.4% (GDH-PQQ), and 95.8 (GDH-FAD) of results were 
within the limits stipulated by ISO15197:2013. All three glucometers showed 
blood glucose results within zones A and B of the consensus error grid, implying 
that it is clinically acceptable, and the Bland-Altman plot showed that the 
GDH-FAD method had the narrowest range between the upper and lower limit of 
agreement and a minimum bias of -0.89. Conclusion Only one test glucometer with 
the GDH-FAD method met the ISO15197:2013 criteria. Glucometers must meet the 
accuracy standards for the safety of the patients.

Copyright © 2024, George et al.

DOI: 10.7759/cureus.70981
PMCID: PMC11539051
PMID: 39507142

Conflict of interest statement: Human subjects: Consent was obtained or waived 
by all participants in this study. Ethics Committee of Amrita School of Medicine 
issued approval ECASM-AIMS-2023-052. The committee reviewed the submitted 
documents of the research protocol. No ethical issues has been observed in the 
study, hence clearance is granted. . Animal subjects: All authors have confirmed 
that this study did not involve animal subjects or tissue. Conflicts of 
interest: In compliance with the ICMJE uniform disclosure form, all authors 
declare the following: Payment/services info: Received grant of 255.53 GBP as 
part of ReachSci Mini PhD programme in collaboration between ReachSci Society 
Cambridge University and Amrita Vishwa Vidyapeetham, Kochi. Financial 
relationships: All authors have declared that they have no financial 
relationships at present or within the previous three years with any 
organizations that might have an interest in the submitted work. Other 
relationships: All authors have declared that there are no other relationships 
or activities that could appear to have influenced the submitted work.


5. J Nanobiotechnology. 2024 Nov 6;22(1):680. doi: 10.1186/s12951-024-02948-w.

Cascade-catalysed nanocarrier degradation for regulating metabolism homeostasis 
and enhancing drug penetration on breast cancer.

Zhang F(#)(1), Cheng K(#)(1), Zhang XS(#)(2), Zhou S(1), Zou JH(1)(3), Tian 
MY(1), Hou XL(1), Hu YG(1), Yuan J(1), Fan JX(4), Zhao YD(5)(6), Liu TC(7)(8).

Author information:
(1)Britton Chance Center for Biomedical Photonics at Wuhan National Laboratory 
for Optoelectronics - Hubei Bioinformatics & Molecular Imaging Key Laboratory, 
Department of Biomedical Engineering, College of Life Science and Technology, 
Huazhong University of Science and Technology, Wuhan, Hubei, 430074, P.R. China.
(2)Basic Medical Laboratory, General Hospital of Central Theater Command, Wuhan, 
Hubei, 430081, P.R. China.
(3)Department of Oncology, Huanggang Central Hospital of Yangtze University, 
Huanggang, Hubei, 438000, P.R. China.
(4)Britton Chance Center for Biomedical Photonics at Wuhan National Laboratory 
for Optoelectronics - Hubei Bioinformatics & Molecular Imaging Key Laboratory, 
Department of Biomedical Engineering, College of Life Science and Technology, 
Huazhong University of Science and Technology, Wuhan, Hubei, 430074, P.R. China. 
jxfan@hust.edu.cn.
(5)Britton Chance Center for Biomedical Photonics at Wuhan National Laboratory 
for Optoelectronics - Hubei Bioinformatics & Molecular Imaging Key Laboratory, 
Department of Biomedical Engineering, College of Life Science and Technology, 
Huazhong University of Science and Technology, Wuhan, Hubei, 430074, P.R. China. 
zydi@mail.hust.edu.cn.
(6)NMPA Research Base of Regulatory Science for Medical Devices & Institute of 
Regulatory Science for Medical Devices, Huazhong University of Science and 
Technology, Wuhan, Hubei, 430074, P.R. China. zydi@mail.hust.edu.cn.
(7)Key Laboratory of Antibody Engineering of Guangdong Higher Education 
Institutes, School of Laboratory Medicine and Biotechnology, Southern Medical 
University, Guangzhou, Guangdong, 510515, P.R. China. liutc@smu.edu.cn.
(8)Guangdong Provincial Key Laboratory of Construction and Detection in Tissue 
Engineering, Southern Medical University, Guangzhou, Guangdong, 510515, P.R. 
China. liutc@smu.edu.cn.
(#)Contributed equally

The abnormal structure of tumor vascular seriously hinders the delivery and deep 
penetration of drug in tumor therapy. Herein, an integrated and tumor 
microenvironment (TME)-responsive nanocarrier is designed, which can dilate 
vessle and improve the drug penetration by in situ releasing nitric oxide (NO). 
Briefly, S-nitroso-glutathione (GSNO) and curcumin (Cur) were encapsulatd into 
the Cu-doped zeolite imidazole framework-8 (Cu-ZIF-8) and modified with 
hyaluronic acid. The nanocarrier degradation in the weakly acidic of TME 
releases Cu2+, then deplete overexpressed intratumourally glutathione and 
transformed into Cu+, thus disrupting the balance between nicotinamide adenine 
dinucleotide phosphate and flavin adenine dinucleotide (NADPH/FAD) during the 
metabolism homeostasis of tumor. The Cu+ can generate highly toxic hydroxyl 
radical through the Fenton-like reaction, enhancing the chemodynamic therapeutic 
effect. In addition, Cu+ also decomposes GSNO to release NO by ionic reduction, 
leading to vasodilation and increased vascular permeability, significantly 
promoting the deep penetration of Cur in tumor. Afterwards, the orderly 
operation of cell cycle is disrupted and arrested in the S-phase to induce tumor 
cell apoptosis. Deep-hypothermia potentiated 2D/3D fluorescence imaging 
demonstrated nanocarrier regulated endogenous metabolism homeostasis of tumor. 
The cascade-catalysed multifunctional nanocarrier provides an approach to treat 
orthotopic tumor.

© 2024. The Author(s).

DOI: 10.1186/s12951-024-02948-w
PMID: 39506777 [Indexed for MEDLINE]