Targeting MicroRNA in myopia: Current insights.

Myopia, the most prevalent eye condition, has sparked notable interest regarding its origin and prevention. MicroRNAs (miRNAs) are short, non-coding RNA strands typically consisting of 18-24 nucleotides. They play a central role in post-transcriptional gene regulation and are closely associated with both normal and pathological processes in organisms. Recent advances in next-generation sequencing and bioinformatics have provided novel insights into miRNA expression and its regulatory role in myopia. This review discusses the distinct expression patterns, regulatory functions, and potential pathways of miRNAs involved in the onset and progression of myopia. The primary objective of this review was to provide valuable insights into molecular mechanisms underlying myopia and the contribution of miRNAs. These insights are expected to pave the way for further exploration of the molecular mechanisms, diagnosis, treatment, and clinical applications of myopia.

Genetic association of PRKCD and CARD9 polymorphisms with Vogt-Koyanagi-Harada disease in the Chinese Han population.

BACKGROUND: Protein kinase C delta (PRKCD) and caspase recruitment domain family member 9 (CARD9) are genes involved in B and T cell activation, and cytokine production, which are vital mechanisms underlying autoimmune disease development. This study aimed to explore the association of the PRKCD and CARD9 genes with Vogt-Koyanagi-Harada disease (VKH) disease. The case-control study was performed to in 912 patients with VKH and 878 normal controls. MassARRAY system, SHEsis online platform, real-time PCR, and enzyme-linked immunosorbent assay were used to detect genotyping, haplotyping, mRNA expression, and cytokine levels, respectively. RESULTS: We found that rs74437127 C allele of PRKCD, rs3812555 CC genotype, and C allele of CARD9 were associated with increased susceptibility of VKH (Pc = 0.020, OR = 1.624; Pc = 2.04 × 10-5, OR = 1.810; Pc = 2.76 × 10-5, OR = 1.698, respectively). However, the rs74437127 T allele, and rs3812555 TC genotype and T allele were linked with decreased susceptibility to VKH (Pc = 0.020, OR = 0.616; Pc = 7.85 × 10-5, OR = 0.559; Pc = 2.76 × 10-5, OR = 0.589, respectively). PRKCD ATG and CARD9 GCTTA haplotypes decreased susceptibility to VKH (Pc = 3.11 × 10-3, OR = 0.594; Pc = 5.00 × 10-3, OR = 0.639, respectively). Functional studies on rs3812555 genotyped individuals revealed that CC carriers had significantly higher CARD9 mRNA expression and tumour necrosis factor-α production than TC/TT carriers (P = 1.00 × 10-4; P = 2.00 × 10-3, respectively). CONCLUSIONS: We found an association between PRKCD rs74437127 and CARD9 rs3812555 polymorphisms and VKH susceptibility and revealed that the increased susceptibility of rs3812555 for VKH may be mediated by regulating CARD9 gene expression and the production of pro-inflammatory cytokines, such as TNF-α.

Circadian rhythm, ipRGCs, and dopamine signalling in myopia.

Myopia, a common ophthalmic disorder, places a high economic burden on individuals and society. Genetic and environmental factors influence myopia progression; however, the underlying mechanisms remain unelucidated. This paper reviews recent advances in circadian rhythm, intrinsically photosensitive retinal ganglion cells (ipRGCs), and dopamine (DA) signalling in myopia and proposes the hypothesis of a circadian rhythm brain retinal circuit in myopia progression. The search of relevant English articles was conducted in the PubMed databases until June 2023. Based on the search, emerging evidence indicated that circadian rhythm was associated with myopia, including circadian genes Bmal1, Cycle, and Per. In both humans and animals, the ocular morphology and physiology show rhythmic oscillations. Theoretically, such ocular rhythms are regulated locally and indirectly via the suprachiasmatic nucleus, which receives signal from the ipRGCs. Compared with the conventional retinal ganglion cells, ipRGCs can sense the presence of light because of specific expression of melanopsin. Light, together with ipRGCs and DA signalling, plays a crucial role in both circadian rhythm and myopia. In summary, regarding myopia progression, a circadian rhythm brain retinal circuit involving ipRGCs and DA signalling has not been well established. However, based on the relationship between circadian rhythm, ipRGCs, and DA signalling in myopia, we hypothesised a circadian rhythm brain retinal circuit.

A Novel Method for Rolling Bearing Fault Diagnosis Based on Gramian Angular Field and CNN-ViT.

Fault diagnosis is one of the important applications of edge computing in the Industrial Internet of Things (IIoT). To address the issue that traditional fault diagnosis methods often struggle to effectively extract fault features, this paper proposes a novel rolling bearing fault diagnosis method that integrates Gramian Angular Field (GAF), Convolutional Neural Network (CNN), and Vision Transformer (ViT). First, GAF is used to convert one-dimensional vibration signals from sensors into two-dimensional images, effectively retaining the fault features of the vibration signal. Then, the CNN branch is used to extract the local features of the image, which are combined with the global features extracted by the ViT branch to diagnose the bearing fault. The effectiveness of this method is validated with two datasets. Experimental results show that the proposed method achieves average accuracies of 99.79% and 99.63% on the CWRU and XJTU-SY rolling bearing fault datasets, respectively. Compared with several widely used fault diagnosis methods, the proposed method achieves higher accuracy for different fault classifications, providing reliable technical support for performing complex fault diagnosis on edge devices.

The role of regulatory T cells in the pathogenesis of acute kidney injury.

The incidence of acute kidney injury (AKI) is on the rise and is associated with high mortality; however, there are currently few effective treatments. Moreover, the relationship between Tregs and other components of the immune microenvironment (IME) in the pathogenesis of AKI remains unclear. We downloaded four publicly accessible AKI datasets, GSE61739, GSE67401, GSE19130, GSE81741, GSE19288 and GSE106993 from the gene expression omnibus (GEO) database. Additionally, we gathered two kidney single-cell sequencing (scRNA-seq) samples from the Department of Organ Transplantation at Zhujiang Hospital of Southern Medical University to investigate chronic kidney transplant rejection (CKTR). Moreover, we also collected three samples of normal kidney tissue from GSE131685. By analysing the differences in immune cells between the AKI and Non-AKI groups, we discovered that the Non-AKI group contained a significantly greater number of Tregs than the AKI group. Additionally, the activation of signalling pathways, such as inflammatory molecules secretion, immune response, glycolytic metabolism, NOTCH, FGF, NF-κB and TLR4, was significantly greater in the AKI group than in the Non-AKI group. Additionally, analysis of single-cell sequencing data revealed that Tregs in patients with chronic kidney rejection and in normal kidney tissue have distinct biology, including immune activation, cytokine production, and activation fractions of signalling pathways such as NOTCH and TLR4. In this study, we found significant differences in the IME between AKI and Non-AKI, including differences in Tregs cells and activation levels of biologically significant signalling pathways. Tregs were associated with lower activity of signalling pathways such as inflammatory response, inflammatory molecule secretion, immune activation, glycolysis.

HES1 deficiency impairs development of human intestinal mesenchyme by suppressing WNT5A expression.

Serious intestinal side-effects that target the NOTCH-HES1 pathway in human cancer differentiation therapy make it necessary to understand the pathway at the human organ level. Herein, we endogenously introduced HES1-/- mutations into human embryonic stem cells (hESCs) and differentiated them into human intestinal organoids (HIO). The HES1-/- hESCs retained ES cell properties and showed gene expression patterns similar to those of wild-type hESCs when they differentiated into definitive endoderm and hindgut. During the formation of the HES1-/- lumen we noted an impaired development of mesenchymal cells in addition to the increased differentiation of secretory epithelium. RNA-Seq revealed that inhibited development of the mesenchymal cells may have been due to a downregulation of WNT5A signaling. Overexpression of HES1 and silencing of WNT5A in the intestinal fibroblast cell line CCD-18Co indicated that HES1 was involved in the activation of WNT5A-induced fibroblast growth and migration, suggesting the likelihood of the Notch pathway in epithelial-mesenchymal crosstalk. Our results facilitated the identification of more precise underlying molecular mechanisms displaying distinct roles in HES1 signaling in stromal and epithelial development in human intestinal mucosa.

Taurine Protects against the Fatty Liver Hemorrhagic Syndrome in Laying Hens through the Regulation of Mitochondrial Homeostasis.

Metabolic-associated fatty liver disease (MAFLD) is a chronic liver disease caused by fat deposition in the liver of humans and mammals, while fatty liver hemorrhagic syndrome (FLHS) is a fatty liver disease in laying hens which can increase the mortality and cause severe economic losses to the laying industry. Increasing evidence has shown a close relationship between the occurrence of fatty liver disease and the disruption of mitochondrial homeostasis. Studies have proven that taurine can regulate hepatic fat metabolism, reduce hepatic fatty deposition, inhibit oxidative stress, and alleviate mitochondrial dysfunction. However, the mechanisms by which taurine regulates mitochondrial homeostasis in hepatocytes need to be further studied. In this study, we determined the effects and mechanisms of taurine on high-energy low-protein diet-induced FLHS in laying hens and in cultured hepatocytes in free fatty acid (FFA)-induced steatosis. The liver function, lipid metabolism, antioxidant capacity, mitochondrial function, mitochondrial dynamics, autophagy, and biosynthesis were detected. The results showed impaired liver structure and function, mitochondrial damage and dysfunction, lipid accumulation, and imbalance between mitochondrial fusion and fission, mitochondrial autophagy, and biosynthesis in both FLHS hens and steatosis hepatocytes. Taurine administration can significantly inhibit the occurrence of FLHS, protect mitochondria in hepatocytes from disease induced by lipid accumulation and FFA, up-regulate the expression levels of Mfn1, Mfn2, Opa1, LC3I, LC3II, PINK1, PGC-1α, Nrf1, Nrf2, and Tfam, and down-regulate the expression levels of Fis1, Drp1, and p62. In conclusion, taurine can protect laying hens from FLHS through the regulation of mitochondrial homeostasis, including the regulation of mitochondrial dynamics, autophagy, and biosynthesis.

Single cell sequencing coupled with bioinformatics reveals PHYH as a potential biomarker in kidney ischemia reperfusion injury.

Ischemia reperfusion injury(IRI) is an important factor affecting the early function and long-term survival of transplanted kidney. Single cell RNA sequencing (scRNA-seq) is a powerful method for investigating cell-specific transcriptome changes in the kidney. This study aimed to identify the significant cell type and potential biomarkers in IRI. First, we downloaded the IRI related scRNA dataset GSE139506 from the GEO database. Then, classification of cell type was characterized and proximal tubule cell (PTC) was identified as a significant cell type. The functional enrichment analysis indicated that PTC were related to kidney function and is significant in the ferroptosis of IRI. Analyses of three-dimensional structure and iron binding substructure of protein was carried out basing on SWISS-MODEL database. Finally, we constructed the murine model with IRI and verify the higher expression of PHYH in IRI by PCR, Western blot (WB) and Immunohistochemistry (IHC) experiments. In conclusion, this study provided novel insights on the cell-type-specific expression gene biomarker in IRI pathogenesis.

Association of CDK6 gene polymorphisms with Behcet's disease in a Han Chinese population.

Cyclin-dependent kinases 4/6 (CDK4/6) and D1-type cyclins (CCND1) can regulate the pro-inflammatory functions of various cytokines during the inflammatory response. This study investigated the association between CDK4/6-CCND1 variants and susceptibility in patients with Behcet's disease (BD). This case-control study enrolled 542 patients with BD and 754 healthy controls. Fourteen tagged single nucleotide polymorphisms (tag SNPs) of the CDK4/6-CCND1 gene were genotyped using the Sequenom MassARRAY system and iPLEX® Pro assay. The results indicated that the frequency of the CDK6 rs2282983 TT genotype was higher in the BD group than the control group (Pc = 0.040, OR = 1.408, 95% CI = 1.124-1.765), and CDK6 rs2282983 CT and rs42034 AG were negatively associated with BD (Pc = 3.647 × 10-4, OR = 0.598, 95% CI = 0.471-0.758; Pc = 0.039, OR = 0.626, 95% CI = 0.459-0.852, respectively). Furthermore, statistical analysis showed that CDK6 rs2282983 TT and CT genotypes were significantly associated with skin lesions in patients with BD (Pc = 0.042, OR = 1.436, 95% CI = 1.130-1.824; Pc = 0.001, OR = 0.594, 95% CI = 0.461-0.764, respectively). This study suggests that the CDK6 loci rs2282983 and rs42034 might confer genetic susceptibility to BD in a Han Chinese population, which could provide new insights into the pathogenesis of BD.

Taurine Prevents AFB1-Induced Renal Injury by Inhibiting Oxidative Stress and Apoptosis.

Aflatoxin B1 (AFB1) is one of the most toxic mycotoxins, which can cause serious kidney damage after ingestion. Taurine protects the kidney, an effect related to its antioxidation and anti-apoptotic actions. In the present study, taurine was administered to detect the protective effect and mechanism of taurine on AFB1-induced renal injury in rats. The results show that taurine ameliorated the increase in serum blood urea nitrogen (BUN), blood creatinine (CRE), blood uric acid (UA), cystatin c (Cys-c), and urinary protein and AKP levels. Taurine also inhibits the content of superoxide dismutase (SOD), total antioxidant capacity (T-AOC), catalase (CAT), glutathione (GSH), glutathione peroxidase (GSH-Px), succinate dehydrogenase (SDH), and the mRNA expression of SOD, nicotinamide adenine dinucleotide phosphate-quinine oxidoreductase 1 (NQO1), γ-glutamylcysteine synthetase (γ-GCS), heme oxygenase-1 (HO-1), and glutamate cysteine ligase catalytic (GCLC) in rat kidney tissue. The apoptotic rate of renal cells was decreased by taurine through inhibition of a mitochondrial mechanism. In summary, we found that taurine prevents AFB1-induced renal injury via enhanced antioxidant ability and mitochondrial-dependent apoptosis.

Taurine Prevents Liver Injury by Reducing Oxidative Stress and Cytochrome C-Mediated Apoptosis in Broilers Under Low Temperature.

Hypoxia caused by low ambient temperature leads to hypoxemia in broilers, which aggravates the metabolic burden of the liver. Liver damage is closely related to oxidative stress and apoptosis. It has been proved that taurine can reduce oxygen free radicals, exert antioxidant properties, and inhibit mitochondria-dependent apoptosis. This experiment aimed to determine whether taurine could prevent liver damage by inhibiting oxidative stress and the cytochrome c-mediated apoptotic pathway in broilers under low ambient temperature. Broilers were given 1% taurine in drinking water, and the temperature was raised at 10 °C ~ 12 °C from 21 to 42 days. At 28 and 42 days, the hepatic tissues were collected. The antioxidant capacity of liver tissues and mRNA expression levels of the factors related with cytochrome c-medicated apoptosis pathway were measured. The results showed taurine significantly increased the total antioxidant capacity (T-AOC) at 28 days. Furthermore, taurine also increased the activities of glutathione peroxidase (GSH-PX) while reducing malondialdehyde (MDA) concentration at 28 days and 42 days. Our results also revealed that taurine significantly increased the mRNA expression levels of Hsp 27 and Hsp 90 while decreasing caspase-3 mRNA expression in broiler hepatocytes at 28 days. In addition, taurine also upregulated the expression level of Bcl-2 at 42 days. In summary, the present study found that taurine enhances the antioxidant ability and alleviates cytochrome c-mediated apoptosis in hepatic tissue of broilers under low temperature.

Antioxidant Effect of Taurine on Chronic Heat-Stressed Broilers.

The purpose of this study was to investigate the effects of taurine on blood indices of broilers with chronic heat stress and to provide theoretical basis for the application of taurine in the anti-chronic heat stress of broilers. In the test, 240 AA + broilers at 7 days of age were randomly divided into five groups: the normal temperature control group (24 ± 2 °C) in group C, the heat stress control group (34 ± 2 °C) in HS group, and the LTau, MTau, and HTau groups in heat under stress conditions, 0.5 g/L, 2 g/L, and 8 g/L taurine, were added to the drinking water, and each group was repeated three times. After 2 weeks of feeding at normal temperature, heat stress began. The test period was 4 weeks. Blood was collected at 6 h, 12 h, 7 d, 14 d, 21 d, and 28 d after heat stress, and serum was separated. The results showed that compared with the HS group, MTau significantly increased the total serum protein content (P < 0.05), but the other groups were not significantly different (P > 0.05). The MTau and HTau groups contained significantly lowered serum uric acid levels than the HS group (P < 0.05). At 7d and 14d, the LTau, MTau, and HTau groups all exhibited significantly increased T3 and T4 concentrations (P < 0.05). There was no significant difference between the groups at other times (P > 0.05). Compared with the HS group, the MTau group contained significantly reduced serum CK activity, LDH activity, AST activity, and ALT activity (P < 0.05). Compared with the LTau, MTau, and HTau groups, serum MDA content was significantly increased in the heat-stressed broilers (P < 0.05). MTau group contained significantly increased T-AOC, SOD, CAT, and GSH-PX levels (P < 0.05). The other groups were not significantly different (P > 0.05). Compared with group C, serum HSP60 and HSP70 levels were significantly elevated in the HS group (P < 0.05). Compared with the HS group, the LTau and MTau groups contained significantly increased serum HSP60 and HSP70 concentrations (P < 0.05), but the other groups were not significantly different (P > 0.05). In conclusion, taurine can alleviate the symptoms of chronic heat stress of broilers, regulate the metabolism of the body, and improve the antioxidant activity of the body.

The Regulatory Effects of Taurine on Neurogenesis and Apoptosis of Neural Stem Cells in the Hippocampus of Rats.

The promotion of neurogenesis from neural stem cells (NSCs) in the hippocampus was found to be the most fundamental and effective therapy for depression. Our previous studies proved an antidepressive effect of taurine on rats, but the exact mechanism remains unclear. In this study, CUMS model was established in rats, and NSCs were cultured in vitro to investigate the protective effect and mechanisms of taurine on neurogenesis and apoptosis in CUMS rats and glutamate-injured NSCs. The results showed that ki67-positive cells were significantly increased by taurine, while apoptosis in the DG of CUMS rats was significantly inhibited by taurine. In vitro study, cell viability, Brdu+, ß-tubulin III+, and GFAP+ cells in taurine-treated cells were significantly higher, while apoptosis rate was lower than the glutamate-treated cells. The protein expression of BDNF and its downstream pathway was upregulated by taurine administration. The results demonstrated that taurine can increase the survival, proliferation, and differentiation of NSCs; this protective effect of taurine may be due to the upregulation of BDNF/ERK/CREB signaling pathway. On the other hand, taurine can also inhibit abnormal apoptosis induced by CUMS or glutamate, the mechanism of which may be due to its antioxidative ability.

Taurine Alleviates LPS-Induced Acute Lung Injury by Suppressing TLR-4/NF-κB Pathway.

Taurine has the function of immune regulation, relieving acute and chronic inflammation caused by various agents, and maintaining cell homeostasis. This investigation focused on the protective functions of taurine targeting acute lung injury (ALI) induced by LPS. Sixty male SD rats aged 6-7 weeks were segregated at random: blank control group (C group), taurine control group (T group), ALI model group (LPS group), and taurine prevention groups (LPST1, LPST, LPST3 Groups). C group and LPS group were given normal drinking water, while T group and LPST group were given 2% taurine in drinking water. LPST1 group was given 1% taurine in drinking water while. LPST3 group was given 3% taurine in drinking water. On the 14th and 28th day, LPS group and LPST1, LPST, and LPST3 groups were subjected to injection of LPS (25 mg/kg) into the trachea of rats. Serum, peripheral blood, lung tissue, and bronchoalveolar lavage fluid (BALF) were collected at 6 h post-LPS injection. The wet/dry ratio (W/D) of lung was measured by hot drying method. The population of white blood cells and the abundance of inflammatory-related cells within peripheral blood were counted by an automatic blood cell analyzer. The population of white blood cells within BALF was counted by a white blood cell counting plate combined with Swiss Giemsa staining, while the proportion of related white blood cells was calculated. BCA reagent was used to determine the protein concentration in BALF. The levels of pro-inflammatory factors (IL-1 ß, IL-6, IL-18, TNF - α), anti-inflammation factors (IL-10, IL-4), and taurine within serum and lung tissue were detected by ELISA. Lung structural tissue alterations were observed through HE staining techniques. Myeloperoxidase (MPO) activities within lung tissue were detected through colorimetry. Protein expression levels of TLR4, MyD88, NF-κ Bp65, NF-κ Bp-p65, MCP-1, together with CD68 within lung tissue, were analyzed by Western blot (WB) and immunohistochemistry (IHC). The taurine pretreatment group contained significantly reduced W/D, MPO activity, and the number of inflammatory cells in BALF induced by LPS. In addition, compared with ALI model group, the taurine pretreatment group contained significantly reduced levels of pro-inflammatory factors in lung tissue, increased levels of anti-inflammatory factors, and decreased expression levels of key proteins in TLR-4/NF-κ B pathway. Taurine can protect rats from ALI by inhibiting the activation of neutrophils, macrophages, and TLR-4/NF-κ B signaling pathway.

Intervention Effect of Taurine on LPS-Induced Intestinal Mechanical Barrier Injury in Piglets.

Taurine has the advantages of being safe, highly efficient, chemically stabile, and biologically active, together with having versatile functions. Presently, it is employed as a veterinary feed additive in animal research. The tight junctions that constitute the intestinal epithelial cells are the most critical structures for ensuring regular and uninterrupted digestion and absorption of food by the intestinal mucosa, while at the same time resisting invasions by toxins. The purpose of this study was to investigate the protective effect and mechanism of taurine action on intestinal mechanical barrier function of piglets that were infected with LPS. The results showed that 0.3% taurine inhibits LPS-driven increase in intestinal permeability and intestinal mucosal injury, the rise in the ratio of villus length to crypt depth within the duodenum, jejunum, and ileum, and the significant enhancement in the expression of tight junction protein-related genes. In summary, dietary taurine significantly reduces intestinal mucosal structural damage and intestinal mucosal permeability while increasing gene expression of tight junction proteins of the intestinal mucosa of piglets induced by LPS, thereby enhancing the effect of intestinal mucosal mechanical barriers.

Effects of Taurine on Serum Indexes of Broilers with Chronic Heat Stress.

The aim of this study was to investigate the effects of taurine on tissue injury, protein metabolism, and basal metabolism of broilers after chronic heat stress by detecting serum physiological and biochemical indices. In the test, 240 AA + broilers at 7 days of age were randomly divided into five groups: the normal temperature control group (24 ± 2 °C) in group C, the heat stress control group (34 ± 2 °C) in HS group, and the LTau, MTau, and HTau groups in heat under stress conditions, 0.5, 2, and 8 g/L taurine were added to the drinking water, and each group was repeated three times. After 2 weeks of feeding at normal temperature, heat stress began. The test period was 4 weeks. Blood was collected at 6 h, 12 h, 7 d, 14 d, 21 d, and 28 d after heat stress, and serum was separated. The results showed that compared with the HS group, the MTau group had significantly higher total serum protein content (P < 0.05), while the other groups were not significantly different (P > 0.05). The MTau and HTau groups had significantly lower serum uric acid levels than the HS group (P < 0.05). At 7d and 14d, the LTau, MTau, and HTau groups all showed significantly increased T3 and T4 concentrations (P < 0.05). There was no significant difference between the groups thereafter (P > 0.05). Compared with HS group, the MTau group contained significantly reduced serum CK activity, LDH activity, AST activity, and ALT activity (P < 0.05). In conclusion, the effects of taurine on tissue damage, protein metabolism, and basal metabolism of broilers after chronic heat stress were studied by measuring serum physiological and biochemical indices. To provide a theoretical basis for the application of taurine in acute heat-stressed broilers.

Taurine Prevents LPS-Induced Liver Injury in Weaned Piglets.

This study employed taurine as a feed additive to explore the prophylactic effect of taurine on LPS-induced hepatic injury in piglets. The pathological shifts within hepatic tissue were observed by HE staining. Serum levels of ALT and AST together with SOD, CAT, GSH-PX activity, and MDA serum and liver levels were detected. TUNEL was used to detect apoptosis, while qPCR was employed to detect HO-1, Nrf-2, Bcl2, BAX, Caspase-3, and NF- κB p65 transcriptomic expression levels. TRL4, Caspase-3, Nrf-2, and NF- κB p-p65/NF- κB p65 were detected by Western blot. The results revealed that taurine reduces LPS-induced pathological damage of hepatic tissue and reduces the levels of ALT and AST in pig serum. The transcriptomic expression levels of HO-1 and Nrf-2 were upregulated, and proteomic expression of Nrf-2 was increased. SOD, CAT, and GSH-PX activity was elevated, while MDA content was reduced in serum and liver. The levels of mRNA of BAX and Caspase-3 were downregulated, but mRNA content of Bcl2 was increased, and the protein levels of TRL4, NF-κB p-p65/NF-κB p65, and Caspase-3 were diminished. Overall, the degree of hepatocyte apoptosis was also significantly reduced. In conclusion, taurine reduces LPS-induced injury of piglet liver, while reducing hepatocyte apoptotic levels. These data provide a scientific basis for the selection of animal feed additives and lay a foundation for the healthy and sustainable development of the porcine industry.

Taurine prevents cardiomyocyte apoptosis by inhibiting the calpain-1/cytochrome c pathway during RVH in broilers.

The calpain-1-activated apoptotic pathway plays a key role in right ventricular hypertrophy (RVH). Taurine has been shown to attenuate apoptosis by inhibiting calpain activity. This experiment aimed to determine whether taurine could prevent RVH by inhibiting the calpain-1/cytochrome c apoptotic pathway. The broilers were given 1% taurine dissolved in drinking water and were raised at 10 °C ~ 12 °C from day 21 to day 42. At 21 d, 28 d, 35 d and 42 d, the right ventricular (RV) tissues were collected. Increased RVH index, angiotensin II, norepinephrine and atrial natriuretic peptide mRNA expression were reduced by taurine in the broiler RVs. Taurine obviously inhibited cardiomyocyte apoptosis via maintaining the mitochondrial membrane potential and decreased the activation of caspase-9 and caspase-3 in the broiler RVs. The antioxidant assay demonstrated that taurine enhanced the activities of superoxide dismutase, total antioxidant capacity and glutathione peroxidase and the glutathione/glutathione disulfide ratio. Western blot results revealed that taurine also downregulated the expression of calpain-1 and cytosolic cytochrome c while upregulating the expression of Bcl-2/Bax and mitochondrial cytochrome c in broiler cardiomyocytes during RVH. In summary, we found that taurine could enhance cardiomyocyte antioxidant ability and further prevented cardiomyocyte apoptosis by inhibiting the calpain-1/cytochrome c pathway during RVH in broilers.

Taurine attenuates isoproterenol-induced H9c2 cardiomyocytes hypertrophy by improving antioxidative ability and inhibiting calpain-1-mediated apoptosis.

Pathological cardiac hypertrophy is ultimately accompanied by cardiomyocyte apoptosis. Apoptosis mainly related to calpain-1-mediated apoptotic pathways. Studies had proved that taurine can maintain heart health through antioxidation and antiapoptotic functions, but the effect of taurine on cardiac hypertrophy is still unclear. This study aimed to determine whether taurine could inhibit calpain-1-mediated mitochondria-dependent apoptotic pathways in isoproterenol (ISO)-induced hypertrophic cardiomyocytes. We found that taurine could inhibit the increase in cell surface area and reduce the protein expression levels of the hypertrophic markers atrial natriuretic peptide, brain natriuretic polypeptide, and ß-myosin heavy chain. Taurine also reduced ROS, intracellular Ca2+ overload and mitochondrial membrane potential. Moreover, taurine inhibited cardiomyocyte apoptosis by decreasing the protein expression of calpain-1, Bax, t-Bid, cytosolic cytochrome c, Apaf-1, cleaved caspase-9 and cleaved caspase-3 and by enhancing calpastatin and Bcl-2 protein expression. Calpain-1 small interfering RNA transfection results showed similar antiapoptotic effects as the taurine prevention group. However, compared with the two treatments, taurine inhibited the expression of cleaved caspase-9 more significantly. Therefore, we believe that taurine prevents ISO-induced H9c2 cardiomyocyte hypertrophy by inhibiting oxidative stress, intracellular Ca2+ overload, the calpain-1-mediated mitochondria-dependent apoptotic pathway and cleaved caspase-9 levels.

PGC1α/CEBPB/CPT1A axis promotes radiation resistance of nasopharyngeal carcinoma through activating fatty acid oxidation.

The PPAR coactivator-1α (PGC1α) is an important transcriptional co-activator in control of fatty acid metabolism. Mitochondrial fatty acid oxidation (FAO) is the primary pathway for the degradation of fatty acids and promotes NADPH and ATP production. Our previous study demonstrated that upregulation of carnitine palmitoyl transferase 1 A (CPT1A), the key regulator of FAO, promotes radiation resistance of nasopharyngeal carcinoma (NPC). In this study, we found that high expression of PGC1α is associated with poor overall survival in NPC patients after radiation treatment. Targeting PGC1α could sensitize NPC cells to radiotherapy. Mechanically, PGC1α binds to CCAAT/enhancer binding protein ß (CEBPB), a member of the transcription factor family of CEBP, to promote CPT1A transcription, resulting in activation of FAO. Our results revealed that the PGC1α/CEBPB/CPT1A/FAO signaling axis promotes radiation resistance of NPC. These findings indicate that the expression of PGC1α could be a prognostic indicator of NPC, and targeting FAO in NPC with high expression of PGC1α might improve the therapeutic efficacy of radiotherapy.