Various devices are used to study the unique electrical properties of acupuncture points (APs), with Voll’s electropuncture diagnostics (EAV) occupying a prominent role. The technical design of EAV allows for the testing of drugs to determine their individual selection and dosages. However, the physiological basis of this phenomenon remains unclear. This study investigated the feasibility of evaluating the electrodermal activity of APs to determine the daily dose of ribavirin using electroacupuncture according to the Voll diagnostic system in patients with long COVID.

This blind, randomized, placebo-controlled trial included 101 patients (aged 16 to 50) who met the definition of long COVID and were examined using an EAV testing system that measures the electrodermal activity of APs. Ribavirin was tested at the APs with established decreased electrical impedance readings to determine the daily doses. Fifty-two participants were randomized to the experimental group, and forty-nine to the placebo group. These patients were considered for data analysis.

The results of this study demonstrated the feasibility of using EAV to identify APs with decreased levels of electrodermal activity, followed by medicament testing (MT) of different ribavirin doses to restore the electrodermal activity at these points.

The results indicated that the tested doses of ribavirin in patients with long COVID correlate with electrodermal activity at certain APs along specific meridians. Higher doses of the drug were associated with lower electrodermal activity readings during MT using the EAV diagnostic system. However, further clinical and instrumental studies are needed to evaluate the clinical application of MT in the assessment of long COVID.

Circular RNAs (circRNAs) are non-coding RNAs characterized by a strictly closed-loop covalent structure. They are abundantly detected in various cells due to their conserved nature. Studies have reported their potential association with chronic liver disease (CLD), including hepatitis, cirrhosis, and hepatocellular carcinoma (HCC), with possible roles as diagnostic and prognostic markers. This study aimed to analyze the potential use of serum-derived hsa_circ_101555 as a diagnostic tool for CLD without HCC, and to compare it with other known non-invasive parameters for liver disease severity and inflammation. Additionally, it aimed to evaluate its expression among non-HCC CLD patients, CLD with HCC cases reported in our published (phase I) study, and healthy controls.

A cross-sectional study (phase II) was conducted involving 30 clinically, laboratory, and radiologically diagnosed Egyptian non-HCC CLD patients and 30 healthy subjects. The serum expression level of hsa_circ_101555 was measured using real-time polymerase chain reaction. The diagnostic accuracy was assessed through receiver operating characteristic curve analysis, calculating the area under the curve to determine sensitivity and specificity. The study also compared hsa_circ_101555 levels with established non-invasive parameters such as the Child-Turcotte-Pugh and model for end-stage liver disease scores, as well as inflammatory markers like the neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio.

hsa_circ_101555 demonstrated high diagnostic accuracy (area under the curve of 0.970) at a cutoff point of 2.088 for differentiating non-HCC CLD patients from healthy controls. Elevated circRNA levels were noted in patients with hepatic encephalopathy and ascites, correlating with advanced liver disease scores (Child-Turcotte-Pugh/model for end-stage liver disease scores). Mean circRNA values were highest in HCC cases, followed by non-HCC CLD patients, and lowest in healthy controls.

Serum-derived hsa_circ_101555 demonstrates high diagnostic accuracy in differentiating non-HCC CLD patients from healthy controls. These findings suggest that hsa_circ_101555 has the potential to serve as a reliable non-invasive biomarker for the early diagnosis of CLD, correlating with disease severity and inflammation markers. Further research with larger sample sizes is warranted to validate its clinical utility and enhance the management of CLD.

Metabolic dysfunction-associated steatohepatitis (MASH) represents a critical step in the progression from simple fatty liver disease to more severe conditions such as cirrhosis and hepatocellular carcinoma, and it remains difficult to treat. Arctigenin (ATG), a monomer of Fructus Arctii, exhibits anti-inflammatory activity. Therefore, we aimed to examine its potential protective role against MASH and explore the underlying mechanisms.

Male C57BL/6 mice were divided into four groups: control, MASH, low-dose ATG (30 mg/kg/day), and high-dose ATG (120 mg/kg/day). MASH was induced through a choline-deficient, L-amino acid-defined high-fat diet for eight weeks, with concurrent preventive ATG administration. Liver injury, lipid metabolism, inflammation, oxidative stress, and fibrosis were assessed. Network pharmacology was employed to identify the potential protective mechanisms of ATG. Key factors were evaluated in vitro to verify the ATG targets.

ATG administration prevented the progression of MASH in a dose-dependent manner. High-dose ATG significantly reduced hepatic macrophage and neutrophil infiltration, serum enzyme levels, and lipid peroxidation, while enhancing antioxidant enzyme activity. Mechanistic network pharmacology identified modulation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome as the central pathway underlying ATG’s bioactivity. Functional analyses in lipopolysaccharide-stimulated RAW264.7 cells confirmed that ATG inhibited NLRP3 expression, pyroptosis-related protein cleavage (hereinafter referred to as GSDMD-N), and pro-inflammatory chemokine production in a concentration-dependent manner. Notably, ATG disrupted NLRP3/GSDMD-N axis activity in macrophages without causing cellular toxicity.

ATG may inhibit the inflammatory cascade primarily by targeting macrophage NLRP3 inflammasomes, thereby preventing the progression of MASH.

MD-1 is a time-tested polyherbal diabetes supplement in Tamil Nadu, India. It is composed of dried powdered herbs: Phyllanthus amarus Schum. & Thonn, Tinospora cordifolia (Willd.) Miers ex Hook. F. & Thoms, Emblica officinalis Gaertn., Eugenia jambolana Lam., Gymnema sylvestre R. Br. Ex, and Cassia auriculata Linn. This study aimed to investigate the in vivo effects of MD-1 in high-fat diet (HFD)-induced diabetes mellitus in C57BL/6J mice.

After 10 weeks of HFD induction, diabetic mice (n = 60) were randomized to 21-day treatments with MD-1, metformin, or left untreated on a standard pellet diet. Fasting blood glucose, triacylglycerol (TAG), total cholesterol, and liver tissue markers including superoxide dismutase, glutathione peroxidase, glutathione, thiobarbituric acid reactive substance, glucokinase, fructose-1,6-bisphosphatase, and glucose-6-phosphatase expressions were measured. Adipose tissue tumor necrosis factor (TNF)-α infiltration and messenger RNA expression of peroxisome proliferator-activated receptor γ (PPAR-γ) and glucose transporter type 4 (Glut4) were also analyzed.

MD-1 treatment significantly reduced elevated fasting blood glucose, TAG, and total cholesterol in HFD-fed mice and countered HFD-induced weight gain despite unchanged caloric intake. Improved adipose tissue function was evidenced by reduced TNF-α infiltration and increased messenger RNA expression of PPAR-γ and Glut4. MD-1 attenuated HFD-induced fatty liver disease by reducing oxidative stress and TAG accumulation, suggesting a possible two-hit mechanism.

MD-1 administration primarily targets adipose tissue TNF-α signaling in HFD mice, restoring function via PPAR-γ/Glut4 expression. These findings support its glycemic intervention potential and justify its supplementation in diabetes.

Sclerocarya birrea (A. Rich) Hochst (Anacardiaceae) is a plant widely used by traditional healers in several African countries to treat numerous illnesses such as Alzheimer’s disease, schizophrenia, inflammation, infections, arterial hypertension, headaches, and others. This study aimed to determine the therapeutic efficacy of Sclerocarya birrea (S. birrea) against glutamate-induced neurotoxicity.

Thirty naïve white mice (Mus musculus Swiss, Muridae), of both genders and weighing between 18 and 25 g, were used in the experiments. Different doses (102.5, 205, and 410 mg/kg) of the extract and vitamin C (100 mg/kg) were administered to the animals one hour before administration of monosodium glutamate (4 mg/kg) for 15 consecutive days. T-maze and Y-maze tests were conducted over three days to assess the animals’ behavioral performance. After behavioral testing, the animals were sacrificed and their brains removed for analysis of oxidative stress parameters.

S. birrea extract reversed glutamate-induced behavioral alterations by significantly (P < 0.001) reducing the latency to reach the platform in the T-maze and significantly increasing the percentage of spontaneous alternation in the Y-maze. The extract also significantly counteracted (P < 0.001) glutamate-induced oxidative stress parameters. The 102.5 and 205 mg/kg doses of the extract significantly (P < 0.001) reduced catalase and reduced glutathione levels, as well as the increase in malondialdehyde levels induced by glutamate.

S. birrea root bark extract exhibits neuroprotective properties that facilitate memory and ameliorate glutamate-induced cognitive deficits in white mice. The results provide partial justification for the traditional medicinal use of S. birrea extract.