Publications by authors named "Jinni Hong"

Background: Studies have revealed extensive taxonomic classifications and patterns of gut microbial diversity in snails, with limited focus on community assembly processes. To better understand the balance between stochastic and deterministic processes in the snail gut microbial assembly and their associations with snail fitness, we used the freshwater snail Biomphalaria straminea as a model and analyzed the gut bacterial communities from 118 samples via high-throughput sequencing of the 16S rRNA gene.

Results: This study reveals that Proteobacteria and Bacteroidota dominate the gut microbiota of B.

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The primary aim of this study was to investigate the alterations in the microbial community of KK-Ay mice following antibiotic treatment. A comparative analysis of the gut microbiota was conducted between KK-Ay mice treated with antibiotics and those without treatment. The microbial community dynamics in antibiotic-treated KK-Ay mice were meticulously assessed over an eight-week period using 16S rDNA sequencing analysis.

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( is a gram-positive anaerobe commonly resides in the human gut microbiota. The advent of metagenomics has linked with various diseases, including inflammatory bowel disease (IBD), obesity, and diabetes mellitus (DM), which has become a growing area of investigation. The initial focus of research primarily centered on assessing the abundance of and its potential association with disease presentation, taking into account variations in sample size, sequencing and analysis methods.

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In this study, we aim to investigate the precise alterations in the gut microbiota during the onset and advancement of diabetic nephropathy (DN) and examine the impact of () on DN. Eight-week-old male KK-Ay mice were administered antibiotic cocktails for a duration of two weeks, followed by oral administration of for an additional eight weeks. Our study revealed significant changes in the gut microbiota during both the initiation and progression of DN.

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The microbiota in the intermediate snail hosts of human schistosomes can significantly affect host biology. For decades, researchers have developed axenic snails to manipulate the symbiotic microbiota. This review summarizes the characteristics of symbiotic microbes in intermediate snail hosts and describes their interactions with snails, affecting snail growth, development, and parasite transmission ability.

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Purpose: This study aimed to elucidate the impact of Jiangtang decoction (JTD) on diabetic kidney disease (DKD) and its association with alterations in the gut microbiota.

Methods: Using a diabetic mouse model (KK-Ay mice), daily administration of JTD for eight weeks was undertaken. Weekly measurements of body weight and blood glucose were performed, while kidney function, uremic toxins, inflammation factors, and fecal microbiota composition were assessed upon sacrifice.

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Background: Studies on the gut microbiota of animals have largely focused on vertebrates. The transmission modes of commensal intestinal bacteria in mammals have been well studied. However, in gastropods, the relationship between gut microbiota and hosts is still poorly understood.

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Background: Gastropoda, the largest class within the phylum Mollusca, houses diverse gut microbiota, and some gastropods serve as intermediate hosts for parasites. Studies have revealed that gut bacteria in gastropods are associated with various biological aspects, such as growth, immunity and host-parasite interactions. Here, we summarize our current knowledge of gastropod gut microbiomes and highlight future research priorities and perspectives.

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snails play a crucial role in the transmission of the human blood fluke . The gut microbiota of intermediate hosts is known to influence their physiological functions, but little is known about its composition and role in snails. To gain insights into the biological characteristics of these freshwater intermediate hosts, we conducted metagenomic sequencing on and to investigate variations in their gut microbiota.

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Background: The role of gut microbiota in diabetes mellitus (DM) and its complications has been widely accepted. However, the alternation of gut microbiota in diabetic microvascular complications (DC) remains to be determined.

Methods: Publications (till August 20, 2022) on gut microbiota in patients with DC were retrieved from PubMed, Web of Science, Embase and Cochrane.

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D-ribose levels are demonstrated to be increased in type II diabetes mellitus and increased blood D-ribose is involved in the development of diabetic complications such as diabetic encephalopathy and nephropathy. However, the mechanism mediating the pathogenic role of D-ribose in nephropathy remains poorly understood. Given that D-ribose was reported to induce advanced glycation end products (AGEs) formation, the present study tested whether D-ribose induces NLRP3 activation and associated glomerular injury via AGEs/receptor of AGEs (RAGE) signaling pathway.

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The glucagon-like peptide-1 (GLP-1) is an insulinotropic hormone secreted by intestinal enteroendocrine L-cells, which plays a crucial role in glucose control, regulation, and protection from different pathological conditions such as diabetes mellitus. The present study sought to test whether GLP-1 release increases gut injury with a high-fat diet (HFD) and whether this GLP-1 release is associated with NLRP3 inflammasome activation. Our results showed that the NLRP3 inflammasome is activated in the intestinal tissue of wild-type mice on a HFD, accompanied by GLP-1 overexpression.

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The transient receptor potential mucolipin 1 (TRPML1) channel has been reported to mediate lysosomal Ca release that is involved in Ca-dependent lysosome trafficking and autophagic flux. However, this regulatory mechanism of lysosomal TRPML1 channel activity in podocytes remains poorly understood. In the present study, we tested whether the TRPML1 channel in podocytes mediates lysosome trafficking, which is essential for multivesicular body (MVB) degradation by lysosomes.

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Recently, it has been found that the level of urinary D-ribose in type 2 diabetes is notably higher than that in age-matched normal control, and D-ribose is more reactive in the glycation than D-glucose and induces oxidative stress. Kaempferol is one of the main bioactive components in , with numerous physiological actives, such as antioxidant. The present study investigated the protective effects of kaempferol on D-ribose-treated mesangial cells.

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The NLRP3 inflammasome is activated in the cytoplasm of cells and its products such as IL-1β are exported through a non-classical ER-Golgi pathway. Several mechanistically distinct models including exocytosis of secretory lysosomes, microvesicles (MVs) and extracellular vehicles (EVs) have been proposed for their release. In this study, we hypothesized that the NLRP3 inflammasome product, IL-1β in response to exogenously administrated and endogenously produced d-ribose stimulation is released via extracellular vesicles including EVs via a sphingolipid-mediated molecular mechanisms controlling lysosome and multivesicular body (MVB) interaction.

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The Nod-like receptor protein 3 (NLRP3) inflammasome activation not only serves as an intracellular machinery triggering inflammation but also produces uncanonical effects beyond inflammation such as changing cell metabolism and increasing cell membrane permeability. The present study was designed to test whether this NLRP3 inflammasome activation contributes to the "two-hit" injury during nonalcoholic steatohepatitis (NASH) and whether it can be a therapeutic target for the action of Fufang Zhenzhu Tiaozhi (FTZ), a widely used herbal remedy for hyperlipidemia and metabolic syndrome in China. We first demonstrated that NLRP3 inflammasome formation and activation as well as lipid deposition occurred in the liver of mice on the high-fat diet (HFD), as shown by increased NLRP3 aggregation, enhanced production of IL-1 and high mobility group box 1 (HMGB1), and remarkable lipid deposition in liver cells.

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Recently, aberrantly high levels of D-ribose have been discovered in type II diabetic patients. D-ribose glycates proteins more rapidly than D-glucose, resulting in the production of advanced glycation end products (AGEs). Accumulations of these products can be found in impaired renal function, but the mechanisms are poorly understood.

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The pannexin-1 (Panx1) channel has been reported to mediate the release of ATP that is involved in local tissue inflammation, obesity, and many chronic degenerative diseases. It remains unknown whether Panx1 is present in podocytes and whether this channel in podocytes mediates ATP release leading to glomerular inflammation or fibrosis. To answer these questions, we first characterized the expression of Panx channels in podocytes.

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To elucidate the efficacy of Jiangtang decoction(JTD) on AGEs-RAGE and oxidative stress in type 2 diabetic model KK-Ay mice. Fifty KK-Ay mice were randomly divided into 5 groups as follows: model group, metformin group, low-dose, medium-dose and high-dose of JTD group, with 10 C57BL/6J as normal group. All groups are orally administrated with equal distilled water, 250 mg•kg⁻¹ metformin hydrochloride, 2, 4,8 g•kg⁻¹ JTD, equal distilled water respectively, once per day for 12 weeks.

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Background: Jiangtang decoction (JTD) is a China patented drug which contains Willd, Bunge, Bunge, Bunge, and Franch. For decades, it has also been used clinically to treat diabetic nephropathy (DN) effectively; however, the associated mechanisms remain unknown. Thus, the present study aimed to examine the protective efficacy of JTD in DN and elucidate the underlying molecular mechanisms.

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Insulin resistance and insulin secretion deficiency are main machanisms in inducing type 2 diabetes mellitus (T2DM), and mitochondria damage plays an important role in them. Research shows that autophagy is a self-protective mechanism of cells, which plays an important role in maintaining the normal structure and function of pancreatic β cells and improving insulin resistance. Previous studies show that traditional Chinese medicine can regulate cell autophagy to influence β cells and insulin resistance, type 2 diabetes mellitus and its complications.

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